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1
acute myelogenous leukemia 2005:2010[pubdate] *count=100
11002 results
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Items 1 to 100 of about 11002
1.
Tsujimura A, Kiyoi H, Shiotsu Y, Ishikawa Y, Mori Y, Ishida H, Toki T, Ito E, Naoe T:
Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in acute myeloid leukemia.
Int J Hematol
; 2010 Nov;92(4):624-33
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[Title]
Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in
acute
myeloid
leukemia
.
Activating mutations of KIT play an important role in the pathophysiology of several human malignancies, including
acute
myeloid
leukemia
.
Here we examined the potency
of a
novel KIT inhibitor KI-328 against different types of mutant KIT kinases recurrently identified in
AML
.
Furthermore, HSP90 inhibitors suppress the growth of D816V-KIT-expressing cells at the concentration at which the growth of other mutant-KIT-expressing cells is
not
affected.
[MeSH-major]
Antineoplastic Agents / pharmacology. Carbamates / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology
[MeSH-minor]
Cell
Line, Tumor. Humans. K562 Cells
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.
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[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Carbamates; 0 / HSP90 Heat-Shock Proteins; 0 / KI 328; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
2.
Mneimneh WS, Bonte H, Bernheim A, Martin A:
Myeloid sarcoma of the prostate revealed by urinary retention: a case report.
BMJ Case Rep
; 2009;2009
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[Title]
Myeloid
sarcoma of the prostate revealed by urinary retention: a case report.
Myeloid
sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.
Here, a singular case
of a
MS of the prostate discovered through investigations for urinary retention and revealing an
acute
leukaemia
classified as an
acute
myeloid leukaemia
(
AML
) with inversion 16 (inv16) according to the World Health Organization (WHO)
classification
(
AML
-M4 with inv16 in the French-American-British (FAB)
classification
) in a 65-year-old man is presented.
None of the previously reported and reviewed cases of prostatic MS were
of AML
-M4 type.
Such a translocation was recently described in some
acute
myeloid
processes.
Radiation therapy could be beneficial for the localised
disease of
the prostate.
Allogenic haematopoietic stem
cell
transplantation is also a promising therapy for MS.
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[ISSN]
1757-790X
[Journal-full-title]
BMJ case reports
[ISO-abbreviation]
BMJ Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC3029613
3.
Yang XP, Li Y, Wang Y, Wang Y, Wang P:
beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in acute myeloid leukemia.
Leuk Lymphoma
; 2010 Aug;51(8):1550-8
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[Title]
beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in
acute
myeloid
leukemia
.
Tryptases are predominantly mast
cell
-specific serine proteases with pleiotropic biological activities.
Recently, significant amounts of tryptases have been shown to be produced by myeloblasts in certain patients with
acute
myeloid
leukemia
(
AML
), but the function of secreted tryptases in pathological circumstances remains unknown.
In this study, we investigated whether beta-tryptase affects the expression of vascular endothelial growth factor (VEGF) in bone marrow stromal cells (BMSCs) in
AML
.
We detected the expression of proteinase-activated receptor-2 (PAR-2) on
AML
BMSCs and found that beta-tryptase significantly up-regulated VEGF mRNA and protein expression in a dose-dependent manner by real-time PCR, Western blot, and ELISA.
These results suggest that beta-tryptase up-regulates VEGF production in
AML
BMSCs via the PAR-2, ERK1/2, and p38MAPK signaling pathways.
[MeSH-major]
Bone Marrow Cells / metabolism.
Leukemia
,
Myeloid
,
Acute
/ metabolism.
Leukemia
, Promyelocytic,
Acute
/ metabolism. Mitogen-Activated Protein Kinases / metabolism. Receptor, PAR-2 / metabolism. Stromal Cells / metabolism. Tryptases / metabolism. Vascular Endothelial Growth Factor A / metabolism
[MeSH-minor]
Blotting, Western.
Cell
Proliferation. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoenzyme Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation
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.
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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 20578818.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.59 / Tryptases
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4.
Kroeger H, Jelinek J, Estécio MR, He R, Kondo K, Chung W, Zhang L, Shen L, Kantarjian HM, Bueso-Ramos CE, Issa JP:
Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.
Blood
; 2008 Aug 15;112(4):1366-73
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[Title]
Aberrant CpG island methylation in
acute
myeloid
leukemia
is accentuated at relapse.
DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in
leukemia
pathophysiology.
Its impact in
leukemia
progression is
not
fully understood.
We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in
leukemia
cell
lines and in patients with
acute
myeloid
leukemia
(
AML
): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.
We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with
AML
, both at
diagnosis
and relapse.
Abnormal methylation was found in 23% to 83% of patients at
diagnosis
and in 47% to 93% at relapse, with CDH13 being the most frequently methylated.
We observed concordance in methylation of several genes, confirming the presence
of a
hypermethylator pathway in
AML
.
DNA methylation levels increased at relapse in 25 of 30 (83%) patients with
AML
.
These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at
diagnosis
and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001).
Our data suggest that DNA methylation is involved in
AML
progression and provide a rationale for the use of epigenetic agents in remission maintenance.
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Oncogene. 2002 Apr 18;21(17):2741-9
[
11965547.001
]
(PMID = 18523155.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2515110
5.
Kim I, Keam B, Lee KH, Kim JH, Oh SY, Ra EK, Yoon SS, Park SS, Kim CS, Park S, Hong YC, Kim BK:
Glutathione S-transferase A1 polymorphisms and acute graft-vs.-host disease in HLA-matched sibling allogeneic hematopoietic stem cell transplantation.
Clin Transplant
; 2007 Mar-Apr;21(2):207-13
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[Title]
Glutathione S-transferase A1 polymorphisms and
acute
graft-vs.-host
disease
in HLA-matched sibling allogeneic hematopoietic stem
cell
transplantation.
We assessed whether the clinical outcomes, including
acute
graft-vs.-host
disease
, of 61 patients with hematological malignancies, following HLA-matched sibling allogeneic stem
cell
transplantation using busulfan/cyclophosphamide conditioning are altered by glutathione S-transferase A1 genotypes.
Globally, grade II-IV
acute
graft-vs.-host
disease
developed in 13 patients (21%).
Grade II-IV
acute
graft-vs.-host
disease
developed in 15.2% of 46 patients with GSTA1*A/*A diplotype and in 40.0% of 15 patients with GSTA1*A/*B or GSTA1*B/*B diplotype (p = 0.04).
Moreover, this relationship between GSTA1*A/*A diplotypes and lower incidence of
acute
graft-vs.-host
disease
was independent of the age, gender, stem
cell
source, and
disease
status.
The incidences of
acute
skin graft-vs.-host
disease
were 7% (3/46) in patients with GSTA1*A/*A and 27% (4/15) in patients without GSTA1*A/*A (p = 0.009, univariate; p = 0.01, multivariate).
Acute
hepatic graft-vs.-host
disease
developed in 6 (13%) of 46 patients with the GSTA1*A/*A diplotype and in 4 (27%) of 15 patients without this diplotype (p = 0.09, univariate; p = 0.12, multivariate).
Ten patients (16%) developed hepatic veno-occlusive
disease
.
No significant difference was found in the incidence of hepatic veno-occlusive
disease
between patients with and without the GSTA1*A/*A diplotype (19.6% vs. 6.7%; p = 0.24).
We conclude that the GSTA1*A/*A diplotype is an independent protective factor against
acute
graft-vs.-host
disease
, especially for skin graft-vs.-host
disease
, and probably for hepatic graft-vs.-host
disease
, in patients using busulfan/cyclophosphamide conditioning.
The identification of glutathione S-transferase A1 genotypes prior to allogeneic stem
cell
transplantation could allow conditioning regimens and graft-vs.-host
disease
prophylaxis to be modified to improve outcome.
[MeSH-major]
Glutathione Transferase / genetics. Graft vs Host
Disease
/ genetics. Hematopoietic Stem
Cell
Transplantation. Polymorphism, Single Nucleotide
[MeSH-minor]
Acute
Disease
. Adult. Female. Genotype. Hepatic Veno-Occlusive
Disease
/ etiology. Humans.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / surgery.
Leukemia
,
Myeloid
/ surgery. Male. Middle Aged. Siblings. Transplantation Conditioning
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(PMID = 17425746.001).
[ISSN]
0902-0063
[Journal-full-title]
Clinical transplantation
[ISO-abbreviation]
Clin Transplant
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
EC 2.5.1.18 / GSTA1 protein, human; EC 2.5.1.18 / Glutathione Transferase
6.
Suzuki K, Irie M, Kadowaki H, Shibata T, Kumagai M, Nishida A:
Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.
J Anim Sci
; 2005 Sep;83(9):2058-65
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[Title]
Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle
area
, backfat thickness, and intramuscular fat content.
Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM
area
(
LMA
), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.
Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with
LMA
.
Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with
LMA
(0.32).
The genetic correlation between
LMA
and DL was positive and high (0.64).
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(PMID = 16100060.001).
[ISSN]
1525-3163
[Journal-full-title]
Journal of animal science
[ISO-abbreviation]
J. Anim. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
9007-34-5 / Collagen
7.
Sedlacek P, Formankova R, Mejstrikova E, Keslova P, Hubacek P, Dobrovolna M, Vrana M, Kupkova L, Pittrova H, Stary J:
Allogeneic stem cell transplantation in children with leukemia using human leukocyte antigen-mismatched unrelated donors.
Pediatr Transplant
; 2008 Feb;12(1):24-31
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[Title]
Allogeneic stem
cell
transplantation in children with
leukemia
using human leukocyte antigen-mismatched unrelated donors.
Allogeneic HSCT is a curative treatment, when chemotherapy fails, for certain malignant
diseases
.
We present our data of HSCT using HLA partially allele-mismatched (7-8/10) UDs in 24 children with
leukemia
.
Acute
GvHD grade II was diagnosed in 70.8% of the patients and grade III-IV in 12.5%.
It enables stable engraftment, good control of GvHD, full reconstitution of immunity, and is
not
connected with unacceptable transplant-related mortality.
[MeSH-major]
Graft vs Host
Disease
/ prevention & control.
Leukemia
/ surgery. Stem
Cell
Transplantation
[MeSH-minor]
Adolescent. Antilymphocyte Serum / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Female. Humans.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / surgery. Male. Tissue Donors. Transplantation Immunology
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.
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(PMID = 18186885.001).
[ISSN]
1397-3142
[Journal-full-title]
Pediatric transplantation
[ISO-abbreviation]
Pediatr Transplant
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antilymphocyte Serum
8.
Møller T, Nielsen OJ, Welinder P, Dünweber A, Hjerming M, Moser C, Kjeldsen L:
Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.
Eur J Haematol
; 2010 Apr;84(4):316-22
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[Title]
Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with
acute
leukaemia
.
Traditionally, patients with
acute
leukaemia
are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.
We have developed an outpatient treatment programme for patients with
acute
leukaemia
incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).
Herein, we report the results of outpatient treatment of 60 patients with
acute
leukaemia
(54 with
acute
myeloid leukaemia
) followed prospectively in the period from March 2004 to 2007.
We conclude that outpatient treatment of patients with
acute
leukaemia
is feasible and safe.
[MeSH-major]
Ambulatory Care / methods. Anti-Infective Agents / administration & dosage.
Leukemia
/ drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies
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.
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.
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(PMID = 20002732.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Infective Agents
9.
Palmisano M, Grafone T, Renzulli M, Ottaviani E, Testoni N, Paolini S, Papayannidis C, Baccarani M, Martinelli G:
Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.
Hematology
; 2008 Feb;13(1):1-12
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[Title]
Molecular and chromosomal alterations: new therapies for relapsed
acute
myeloid
leukemia
.
Acute
myeloid
leukemia
(
AML
) remains the most common form of
leukemia
and the most common cause of
leukemia
death.
Although conventional chemotherapy can cure between 25 and 45%
of AML
patients, the majority of patients die after relapse or of complications associated with treatment.
Thus, more specific and less toxic treatments
for AML
patients are needed, especially for elderly patients.
An indispensable prerequisite to investigate tailored approaches
for AML
is the recent progress in the understanding the molecular features that distinguish
leukemia
progenitors from normal hematopoietic counterparts and the identification
of a
variety of dysregulated molecular pathways.
In this review, we describe some of the signaling pathways that are aberrantly regulated in
AML
, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects
[MeSH-minor]
Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to
Disease
/ genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic
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(PMID = 18534059.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
[Number-of-references]
126
10.
Cornely OA, Maertens J, Winston DJ, Perfect J, Ullmann AJ, Walsh TJ, Helfgott D, Holowiecki J, Stockelberg D, Goh YT, Petrini M, Hardalo C, Suresh R, Angulo-Gonzalez D:
Posaconazole vs. fluconazole or itraconazole prophylaxis in patients with neutropenia.
N Engl J Med
; 2007 Jan 25;356(4):348-59
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BACKGROUND: Patients with neutropenia resulting from chemotherapy for
acute myelogenous leukemia
or the myelodysplastic syndrome are at high risk for difficult-to-treat and often fatal invasive fungal infections.
CONCLUSIONS: In patients undergoing chemotherapy for
acute myelogenous leukemia
or the myelodysplastic syndrome, posaconazole prevented invasive fungal infections more effectively than did either fluconazole or itraconazole and improved overall survival.
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Female. Humans. Kaplan-Meier Estimate.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ mortality. Male. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / mortality. Single-Blind Method. Treatment Outcome
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.
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(subscription/membership/fee required).
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Itraconazole
.
Hazardous Substances Data Bank.
FLUCONAZOLE
.
SciCrunch.
DrugBank: Data: Chemical
.
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[Copyright]
Copyright 2007 Massachusetts Medical Society.
[CommentIn]
Nat Clin Pract Oncol. 2007 Sep;4(9):512-3
[
17646862.001
]
[CommentIn]
Curr Infect Dis Rep. 2007 Nov;9(6):446-7
[
17999879.001
]
[CommentIn]
N Engl J Med. 2007 May 24;356(21):2215; author reply 2215-8
[
17526089.001
]
[CommentIn]
N Engl J Med. 2007 May 24;356(21):2214-5; author reply 2215-8
[
17526090.001
]
[CommentIn]
N Engl J Med. 2007 May 24;356(21):2214; author reply 2215-8
[
17522407.001
]
[CommentIn]
N Engl J Med. 2007 Jan 25;356(4):409-11
[
17251538.001
]
(PMID = 17251531.001).
[ISSN]
1533-4406
[Journal-full-title]
The New England journal of medicine
[ISO-abbreviation]
N. Engl. J. Med.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00044486
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 8VZV102JFY / Fluconazole
11.
Kang HJ, Hong SH, Kim IH, Park BK, Han KS, Cho HI, Shin HY, Ahn HS:
Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.
Leuk Res
; 2005 Jun;29(6):617-23
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[Title]
Prognostic significance of FLT3 mutations in pediatric
non
-promyelocytic
acute
myeloid
leukemia
.
This is the first study of FLT3 mutations in pediatric
non
-promyelocytic
AML
patients that received the same treatment scheme in single institute.
Patients with FLT3/TKD remain alive after autologous stem
cell
transplantation.
The
disease
-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).
New therapeutic scheme such as stem
cell
transplantation with more intensive conditioning just after complete remission could be applied in pediatric
non
-promyelocytic
AML
patients with the FLT3/ITD mutation.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
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(PMID = 15863200.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
12.
Guzman ML, Jordan CT:
Feverfew: weeding out the root of leukaemia.
Expert Opin Biol Ther
; 2005 Sep;5(9):1147-52
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[Title]
Feverfew: weeding out the root
of leukaemia
.
Malignant stem cells are central to the pathogenesis and perpetuation of
acute myelogenous
leukaemia
(
AML
).
Despite their crucial role, standard chemotherapy often does
not
target these critical cells and, thus, the 'root' of leukaemic
disease
is
not
eradicated.
To derive better therapies, unique molecular features of malignant stem cells have been characterised
for AML
and evaluated with regard to ablation
of disease
.
In the course of such studies, the compound parthenolide, which is derived from the medicinal plant feverfew, has recently been shown to preferentially induce
AML
stem cells to undergo apoptosis.
Thus, this naturally occurring agent may provide new avenues of investigation for the treatment
of leukaemia
.
[MeSH-major]
Antineoplastic Agents, Phytogenic / pharmacology.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Neoplastic Stem Cells / drug effects. Sesquiterpenes / pharmacology. Tanacetum parthenium / chemistry
[MeSH-minor]
Animals. Apoptosis.
Cell
Line, Tumor. Humans. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Plants, Medicinal / chemistry. Xenograft Model Antitumor Assays
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(PMID = 16120045.001).
[ISSN]
1744-7682
[Journal-full-title]
Expert opinion on biological therapy
[ISO-abbreviation]
Expert Opin Biol Ther
[Language]
eng
[Publication-type]
Editorial
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide
13.
Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H:
High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
Blood
; 2009 May 28;113(22):5583-7
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[Title]
High frequency of RUNX1 biallelic alteration in
acute
myeloid
leukemia
secondary to familial platelet
disorder
.
Familial platelet
disorder
(FPD), a rare autosomal dominant
disorder
characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to
acute
myeloid
leukemia
(
AML
).
So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at
acute leukemia
(AL) stage has shown no additional RUNX1
abnormality
.
In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6
AML
cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to
AML
.
[MeSH-major]
Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
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.
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.
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.
SciCrunch.
OMIM: Data: Gene Annotation
.
SciCrunch.
Clinical Genomic Database: Data: Gene Annotation
.
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(PMID = 19357396.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
14.
Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP:
JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.
Blood
; 2005 Nov 15;106(10):3370-3
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[Title]
JAK2 mutation 1849G>T is rare in
acute
leukemias
but can be found in CMML, Philadelphia chromosome-negative CML, and
megakaryocytic
leukemia
.
The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in
acute
myeloid
leukemia
(
AML
) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).
JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic
myelogenous leukemia
(CML), 2 (18%) of 11 patients with
megakaryocytic AML
, 7 (13%) of 52 patients with chronic myelomonocytic
leukemia
, and 1 (1%) of 68 patients with myelodysplastic syndromes.
No mutation was found in Ph(+)CML (99 patients),
AML M0
-M6 (28 patients), or
acute
lymphoblastic
leukemia
(20 patients).
We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but
not
critical for transformation to the
acute
phase of these
diseases
and that it is generally rare in aggressive
leukemias
.
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[Cites]
Anal Biochem. 2000 Apr 10;280(1):103-10
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Blood. 2002 Feb 1;99(3):840-9
[
11806985.001
]
(PMID = 16037387.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50CA100632
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
[Other-IDs]
NLM/ PMC1895065
15.
Zong N, Adjouadi M, Ayala M:
Optimizing the classification of acute lymphoblastic leukemia and acute myeloid leukemia samples using artificial neural networks.
Biomed Sci Instrum
; 2006;42:261-6
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[Title]
Optimizing the
classification of
acute
lymphoblastic
leukemia
and
acute
myeloid
leukemia
samples using artificial neural networks.
Accurate
classification of
human blood cells plays a decisive role in the
diagnosis
and treatment
of diseases
.
Artificial Neural Networks (ANN) have been consistently used as a trusted
classification
tool for this type of analysis.
In this study, a new Artificial Neural Network approach is proposed for the multidimensional
classification of
two of the most common forms of
leukemia
:
Acute
Lymphoblastic
Leukemia
(ALL) and
Acute
Myeloid
Leukemia
(
AML
), also sometimes called
Acute Myelogenous Leukemia
.
The goal was to establish a programming tool, supported through this new ANN development, for the identification of normal and abnormal blood samples and provide information to medical doctors in the form of diagnostic references for the specific
disease
state that is considered for this study.
The application of the ANN algorithm produced remarkable
classification
accuracy results that show a 95%
classification
accuracy for the normal blood samples and 90%
classification
accuracy for the abnormal samples even under the ubiquitous problem of overlap.
[MeSH-major]
Blood
Cell
Count / methods.
Diagnosis
, Computer-Assisted / methods.
Leukemia
,
Myeloid
,
Acute
/ blood.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Neural Networks (Computer). Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / blood. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
[MeSH-minor]
Blood Cells /
classification
. Cluster Analysis. Humans. Pattern Recognition, Automated / methods. Quality Control. Reproducibility of Results. Sensitivity and Specificity
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.
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.
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.
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consumer health - Blood Count Tests
.
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(PMID = 16817618.001).
[ISSN]
0067-8856
[Journal-full-title]
Biomedical sciences instrumentation
[ISO-abbreviation]
Biomed Sci Instrum
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
16.
Pyatt DW, Aylward LL, Hays SM:
Is age an independent risk factor for chemically induced acute myelogenous leukemia in children?
J Toxicol Environ Health B Crit Rev
; 2007 Sep-Oct;10(5):379-400
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[Title]
Is age an independent risk factor for chemically induced
acute myelogenous leukemia
in children?
Secondary or therapy-related
acute myelogenous leukemia
(t-
AML
) is a rare but unfortunate consequence of treatment with certain classes of cytotoxic chemotherapeutic agents or chronic exposure to high concentrations of benzene.
Drugs known to produce
AML
following chemotherapy of primary malignancy are usually alkylating agents or topoisomerase II inhibitors.
Both children and adults develop
AML
following treatment with these classes of antineoplastic drugs.
In this review, the effect of age at treatment on a child's susceptibility to developing therapy related
AML
was investigated.
As demonstrated in the published literature, the risk of developing
AML
following chemotherapy is
not
reliably correlated with the age of the pediatric patient.
For example, secondary solid tumors such as breast, central nervous system (CNS), bone, and thyroid cancer are highly dependent on the age of the patient at time
of diagnosis
and treatment; in contrast, an age dependency for t-
AML
risk was
not
observed in these same patient populations.
Predictably, the induction of t-
AML
in children follows a rational dose-response relationship, with increasing doses of chemotherapy resulting in greater risk. Recent U.S.
Available scientific and medical literature does
not
support the hypothesis that children necessarily possess an increased risk of developing
AML
following leukemogenic chemical exposure.
[MeSH-major]
Antineoplastic Agents, Alkylating / adverse effects.
Leukemia
,
Myeloid
,
Acute
/ chemically induced.
Leukemia
,
Myeloid
,
Acute
/ epidemiology. Neoplasms, Second Primary / epidemiology
[MeSH-minor]
Adolescent. Age Factors. Child. Child, Preschool.
Disease
Susceptibility. Humans. Risk Factors. Topoisomerase II Inhibitors
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(PMID = 17687725.001).
[ISSN]
1521-6950
[Journal-full-title]
Journal of toxicology and environmental health. Part B, Critical reviews
[ISO-abbreviation]
J Toxicol Environ Health B Crit Rev
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
[Number-of-references]
92
17.
Papamanthos MK, Kolokotronis AE, Skulakis HE, Fericean AM, Zorba MT, Matiakis AT:
Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.
Head Neck Pathol
; 2010 Jun;4(2):132-5
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[Title]
Acute
myeloid leukaemia
diagnosed by intra-oral
myeloid
sarcoma. A case report.
Myeloid
sarcoma (MS) is a rare extramedullary malignant tumor composed of immature
myeloid
cells.
It is strongly associated with a well known or covert
acute
myeloid leukaemia
, chronic myeloproliferative
diseases
or myelodysplastic syndromes.
An unusual case of
acute
myeloid leukaemia
, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.
The histological examination (including immunohistochemical analysis)
of a
subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.
This
lesion
was therefore classified as
acute
myeloid leukaemia
.
The patient was referred to oncologists that confirmed the initial
diagnosis
.
Forty days later, a relapse of the
disease
, which appeared as a great-ulcerated
lesion
, was developed in the hard palate.
Review of the literature shows no report of intraoral relapse and particularly multiple relapse
of a
MS that involves the oral cavity.
Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential
diagnosis of
conditions (especially tumors) with a similar clinical appearance.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Neoplasms, Multiple Primary /
diagnosis
. Sarcoma,
Myeloid
/
diagnosis
[MeSH-minor]
Aged. Antineoplastic Agents / therapeutic use. Biopsy.
Diagnosis
, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms
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.
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.
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[Cites]
J Oral Maxillofac Surg. 1990 Jul;48(7):748-52
[
2193130.001
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Leuk Res. 2004 Jan;28(1):25-34
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Quintessence Int. 2007 Nov-Dec;38(10):817-20
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Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Jan;105(1):e34-6
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Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 Jun;103(6):e44-8
[
17428693.001
]
(PMID = 20512638.001).
[ISSN]
1936-0568
[Journal-full-title]
Head and neck pathology
[ISO-abbreviation]
Head Neck Pathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide
[Other-IDs]
NLM/ PMC2878628
18.
Renneville A, Boissel N, Zurawski V, Llopis L, Biggio V, Nibourel O, Philippe N, Thomas X, Dombret H, Preudhomme C:
Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.
Cancer
; 2009 Aug 15;115(16):3719-27
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[Title]
Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with
acute
myeloid
leukemia
: a study from the
Acute Leukemia
French Association.
BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most
acute
myeloid leukemias
(
AMLs
).
Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype
AMLs
and are an independent predictor of poor outcome in this subgroup of patients with
AML
.
METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with
AML
who were treated on the
Acute Leukemia
French Association 9802 trial.
Within the subgroup of patients who had normal karyotype
AML
(n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.
CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with
AML
.
Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with
AML
.
[MeSH-major]
Genes, Wilms Tumor.
Leukemia
,
Myeloid
,
Acute
/ genetics
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(PMID = 19536888.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
19.
Rawat VP, Thoene S, Naidu VM, Arseni N, Heilmeier B, Metzeler K, Petropoulos K, Deshpande A, Quintanilla-Martinez L, Bohlander SK, Spiekermann K, Hiddemann W, Feuring-Buske M, Buske C:
Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.
Blood
; 2008 Jan 1;111(1):309-19
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[Title]
Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human
acute
myeloid
leukemia
.
The mechanisms underlying deregulation of HOX gene expression in
AML
are poorly understood.
Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause
acute
myeloid
leukemia
(
AML
) in mice.
In contrast inactivation of the putative Pbx interacting site of Cdx2 did
not
change the leukemogenic potential of the gene.
In an analysis of 115 patients with
AML
, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.
All patients with
AML
with normal karyotype tested were negative for CDX1 and CDX4 expression.
They furthermore correlate the level of CDX2 expression with HOX gene expression in human
AML
and support a potential role of CDX2 in the development of human
AML
with aberrant Hox gene expression.
[MeSH-major]
Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Transcription Factors / genetics
[MeSH-minor]
Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation.
Cell
Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology
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(PMID = 17855634.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
20.
Yang L, Zhang Y, Zhang MR, Xiao ZJ:
[Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
Zhonghua Yi Xue Za Zhi
; 2005 Aug 31;85(33):2312-6
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[Title]
[Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and
acute
myeloid
leukemia
and recurrent chromosome translocations].
OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to
acute
myeloid
leukemia
(
AML
) and recurrent chromosome translocations
of AML
.
METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with
de
novo
AML
and 241 controls by PCR or PCR-RFLP.
RESULTS: The frequency of GSTM1 null genotype in the
AML
patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.
The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total
AML
patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the
AML
patients with t (8;.
21) (q22; q22)/
AML
-ETO fusion gene, and 57.1% and 26.0% respectively among the
AML
patient with t (15;.
21) (q22; q22)/
AML
-ETO (+)
AML
was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.
17) (q22; q11)/PML-RARalpha (+)
AML
was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.
CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals
for AML
, especially
for AML
with t (8;.
21) (q22; q22)/
AML
-ETO fusion gene and t (15;.
[MeSH-major]
Chromosome Aberrations. Glutathione Transferase / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
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(PMID = 16321221.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
21.
Mann C, Parkinson N, Bleetman A:
Endotracheal tube and laryngeal mask airway cuff volume changes with altitude: a rule of thumb for aeromedical transport.
Emerg Med J
; 2007 Mar;24(3):165-7
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Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (
LMAs
).
The cuffs of both ETTs and
LMAs
inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).
METHODS: The change in dimensions of the inflated cuffs
of a
size 8 ETT and a size 5
LMA
were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.
RESULTS:
A linear
expansion in cuff dimensions as a function of altitude increase was identified.
CONCLUSION: The data
for LMA
cuff expansion failed to show significant correlation with altitude change.
Further work is required to determine a similar rule of thumb
for LMA
cuff deflation.
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[Cites]
Anaesthesia. 2000 Dec;55(12):1179-84
[
11121927.001
]
[Cites]
Anaesthesia. 2002 Apr;57(4):374-8
[
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]
[Cites]
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10452473.001
]
[CommentIn]
Emerg Med J. 2007 Aug;24(8):605
[
17652705.001
]
(PMID = 17351218.001).
[ISSN]
1472-0213
[Journal-full-title]
Emergency medicine journal : EMJ
[ISO-abbreviation]
Emerg Med J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2660019
22.
Beluffi G, Bernardo ME, Meloni G, Spinazzola A, Locatelli F:
Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.
Pediatr Radiol
; 2008 Jun;38(6):709-12
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[Title]
Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem
cell
transplantation.
We report the case
of a
child affected by
acute
myeloid leukaemia
who was treated with allogeneic haematopoietic stem
cell
transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.
The
diagnosis
was difficult on a clinical basis, but made possible by conventional radiography and MRI.
[MeSH-major]
Aspergillosis / complications. Hematopoietic Stem
Cell
Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal
Diseases
/ microbiology
[MeSH-minor]
Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage.
Diagnosis
, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant.
Leukemia
,
Myeloid
,
Acute
/ surgery. Magnetic Resonance Imaging. Male. Radiography. Rare
Diseases
. Recurrence. Spine / diagnostic imaging. Spine / pathology
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[Cites]
Pediatr Radiol. 2003 Jul;33(7):453-60
[
12739082.001
]
[Cites]
Clin Infect Dis. 1998 Apr;26(4):781-803; quiz 804-5
[
9564455.001
]
[Cites]
J Infect. 2000 Jul;41(1):97-100
[
11041713.001
]
[Cites]
Blood. 2002 Dec 15;100(13):4358-66
[
12393425.001
]
[Cites]
Acta Orthop Belg. 1993;59(3):306-14
[
8237349.001
]
[Cites]
Pediatrics. 1994 May;93(5):830-5
[
8165091.001
]
[Cites]
Pediatr Neurosurg. 2001 Jul;35(1):18-23
[
11490186.001
]
[Cites]
Clin Infect Dis. 2001 Jan;32(1):9-16
[
11112668.001
]
(PMID = 18392819.001).
[ISSN]
0301-0449
[Journal-full-title]
Pediatric radiology
[ISO-abbreviation]
Pediatr Radiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
23.
Kohlschütter J, Michelfelder S, Trepel M:
Drug delivery in acute myeloid leukemia.
Expert Opin Drug Deliv
; 2008 Jun;5(6):653-63
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[Title]
Drug delivery in
acute
myeloid
leukemia
.
BACKGROUND:
Acute
myeloid
leukemia
was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.
OBJECTIVE: We have chosen
acute
myeloid
leukemia
as
a disease
prototype to review established and novel targeted approaches in
leukemia
treatment.
CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation for
leukemia
-directed uptake, their efficacy has probably
not
changed significantly.
Further improvements may result from the characterization of novel
acute
myeloid
leukemia
(
AML
)
cell
surface receptors and of leukemic stem cells, as well as from the design of
leukemia
-targeted gene therapy vectors.
[MeSH-minor]
Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 18532921.001).
[ISSN]
1742-5247
[Journal-full-title]
Expert opinion on drug delivery
[ISO-abbreviation]
Expert Opin Drug Deliv
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3
[Number-of-references]
114
24.
Vyas HK, Pal R, Vishwakarma R, Lohiya NK, Talwar GP:
Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
Oncology
; 2009;76(2):101-11
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[Title]
Selective killing of
leukemia
and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of
acute
myeloid
leukemia
(
AML
) patients.
RESULTS: The antibody did
not
impair the growth of MOLT-4 and U-937 cells in culture.
Its conjugate with curcumin, however, was lethal to both
cell
lines.
The immunoconjugate killed tumor cells bearing the CD33 marker of an
AML
patient expressing hCGbeta but did
not
have a similar action on cells of another
AML
patient with the CD13 marker but who was negative for hCGbeta.
[MeSH-major]
Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism.
Leukemia
/ drug therapy. Lymphoma / drug therapy
[MeSH-minor]
Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis.
Cell
Separation. Drug Design. Female. Humans.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells
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.
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METHYLTHIAZOLETETRAZOLIUM
.
Hazardous Substances Data Bank.
CURCUMIN
.
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(PMID = 19127081.001).
[ISSN]
1423-0232
[Journal-full-title]
Oncology
[ISO-abbreviation]
Oncology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
25.
Raffegerst SH, Hoelzlwimmer G, Kunder S, Mysliwietz J, Quintanilla-Martinez L, Schendel DJ:
Diverse hematological malignancies including hodgkin-like lymphomas develop in chimeric MHC class II transgenic mice.
PLoS One
; 2009;4(12):e8539
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The majority of malignancies were distributed equally between T and B
cell
neoplasms and included
lymphoblastic
T
cell
lymphoma (LTCL),
lymphoblastic
B
cell
lymphoma (LBCL), diffuse large B
cell
lymphoma (DLBCL), the histiocyte/T
cell
rich variant of DLBCL (DLBCL-HA/T
cell
rich DLBCL), splenic marginal zone lymphoma (SMZL), follicular B
cell
lymphoma (FBL) and plasmacytoma (PCT).
Most of these neoplasms were highly similar to human
diseases
.
Also, some
non
-lymphoid malignancies such as
acute
myeloid
leukemia
(
AML
) and histiocytic sarcoma were found.
Interestingly, composite lymphomas, including Hodgkin-like lymphomas, were also detected that had CD30(+) Hodgkin/Reed-Sternberg (H/RS)-like cells, representing a tumor type
not
previously described in mice.
Thus, this DR4 line is a useful model to investigate common molecular mechanisms that may contribute to important neoplastic
diseases
in man.
[MeSH-major]
Chimerism. Hematologic Neoplasms / immunology. Hematologic Neoplasms / pathology. Histocompatibility Antigens Class II / immunology. Hodgkin
Disease
/ immunology. Hodgkin
Disease
/ pathology
[MeSH-minor]
Animals. Antigens, CD30 / metabolism. Base Sequence. Lymphoma, B-
Cell
/ pathology. Lymphoma, T-
Cell
/ pathology. Mice. Mice, Transgenic. Molecular Sequence Data. Reed-Sternberg Cells / pathology. Survival Analysis. Transgenes / genetics
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.
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[Cites]
Blood. 2002 Jul 1;100(1):238-45
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Blood. 2002 Jul 1;100(1):246-58
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12070034.001
]
(PMID = 20046882.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD30; 0 / Histocompatibility Antigens Class II
[Other-IDs]
NLM/ PMC2796171
26.
Calvo D, Cariddi LN, Grosso M, Demo MS, Maldonado AM:
Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.
Rev Latinoam Microbiol
; 2006 Jul-Dec;48(3-4):247-55
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[Title]
Achyrocline satureioides (
LAM
.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.
Achyrocline satureioides (
LAM
.
They were isolated from 18 patients with acne
lesions
and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).
On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control
non
-infected individuals.
The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the
lymphocyte
expansion, of which 40% were CD8+ T cells.
[MeSH-minor]
Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans.
Lymphocyte
Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology
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(PMID = 18293658.001).
[ISSN]
0187-4640
[Journal-full-title]
Revista latinoamericana de microbiología
[ISO-abbreviation]
Rev. Latinoam. Microbiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Mexico
[Chemical-registry-number]
0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts
27.
Senatore F, Arnold NA, Bruno M:
Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.
Nat Prod Res
; 2005 Dec;19(8):749-54
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[Title]
Volatile components of Centaurea eryngiodes
Lam
. and Centaurea iberica Trev.var. hermonis Bois.
Lam
.,two Asteraceae growing wild in Lebanon.
The volatile components of the flowerheads of Centaurea eryngioides
Lam
. and Centaurea iberica Trev. var. hermonis Boiss.
Lam
. were obtained by hydrodistillation and identified by GC and GC-MS.
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(PMID = 16317829.001).
[ISSN]
1478-6419
[Journal-full-title]
Natural product research
[ISO-abbreviation]
Nat. Prod. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Oils, Volatile; 0 / Plant Oils
28.
Konoplev S, Huang X, Drabkin HA, Koeppen H, Jones D, Kantarjian HM, Garcia-Manero G, Chen W, Medeiros LJ, Bueso-Ramos CE:
Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis.
Cancer
; 2009 Oct 15;115(20):4737-44
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[Title]
Cytoplasmic localization of nucleophosmin in bone marrow blasts of
acute
myeloid
leukemia
patients is
not
completely concordant with NPM1 mutation and is
not
predictive of prognosis.
BACKGROUND: Nucleophosmin (NPM1) gene mutations are reported to predict a favorable prognosis in
acute
myeloid
leukemia
(
AML
) patients.
RESULTS: The study included 252
AML
patients: 192
de
novo
AML
, 33
AML
preceded by either myelodysplastic syndrome or chronic myelomonocytic
leukemia
, and 27 therapy-related
AML
.
Cytoplasmic NPM was detected in 59 of 252 (23%) patients, including 48 of 192 (25%)
de
novo
AML
and 33 of 94 (35%) with a normal karyotype.
CONCLUSIONS: IHC assessment for NPM localization did
not
predict prognosis in this patient cohort.
[MeSH-major]
Bone Marrow / metabolism. Cytoplasm / metabolism.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism
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[Copyright]
Copyright (c) 2009 American Cancer Society.
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[Cites]
Am J Clin Pathol. 2001 Dec;116(6):886-92
[
11764078.001
]
(PMID = 19637342.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / U54 CA096300
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
[Other-IDs]
NLM/ NIHMS633932; NLM/ PMC4199225
29.
Kuchenbauer F, Kern W, Schoch C, Kohlmann A, Hiddemann W, Haferlach T, Schnittger S:
Detailed analysis of FLT3 expression levels in acute myeloid leukemia.
Haematologica
; 2005 Dec;90(12):1617-25
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[Title]
Detailed analysis of FLT3 expression levels in
acute
myeloid
leukemia
.
BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of
acute
myeloid
leukemia
(
AML
).
DESIGN AND METHODS: To further evaluate the role of FLT3 in
AML
we investigated FLT3 expression levels in 207 adult
AML
patients and 8 healthy donors by real-time polymerase chain reaction (PCR).
RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<
M2
<M4eo<M4<
M0
<
M1
<M5a<M5b.
Independent analysis of FLT3 expression in cytogenetic
AML
subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive
AML
.
On the molecular level, no differences in FLT3 expression levels were detected between
AML
with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).
In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency
for a
worse overall (p=0.059) and event free (p=0.087) survival was found.
[MeSH-major]
Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
/ enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations.
Disease
-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping.
Leukemia
, Monocytic,
Acute
/ genetics.
Leukemia
, Monocytic,
Acute
/ pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences
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.
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NCI CPTAC Assay Portal
.
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[CommentIn]
Haematologica. 2005 Dec;90(12):1586
[
16330422.001
]
(PMID = 16330434.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
30.
Parikh SA, Kadia T, Jabbour E:
Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.
Clin Lymphoma Myeloma Leuk
; 2010 Aug;10(4):301-2
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[Title]
Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor
acute
myeloid
leukemia
: more than meets the eye.
The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor
acute
myeloid
leukemia
(
AML
).
A side effect of administration
of G
-CSF is an increase in peripheral white blood
cell
count and blast
cell
percentage during the recovery phase of the bone marrow after induction chemotherapy.
A 60-year-old man with inversion 16
AML
was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.
Our case report underscores the importance of recognizing this phenomenon associated with the administration
of G
-CSF, and waiting for 5-7 days before administering
re
-induction therapy or classifying the
disease
as primary refractory
AML
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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(PMID = 20709669.001).
[ISSN]
2152-2669
[Journal-full-title]
Clinical lymphoma, myeloma & leukemia
[ISO-abbreviation]
Clin Lymphoma Myeloma Leuk
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol
31.
Kessler T, Fehrmann F, Bieker R, Berdel WE, Mesters RM:
Vascular endothelial growth factor and its receptor as drug targets in hematological malignancies.
Curr Drug Targets
; 2007 Feb;8(2):257-68
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With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration of
leukemia
cells could be demonstrated.
Bone marrow of
leukemia
patients shows an increased microvessel density as well as VEGF expression.
Complete remissions in
acute
myeloid
leukemia
(
AML
) have been reported by targeting the receptor tyrosine kinase system of VEGF.
While the pathophysiology behind the contribution of VEGF to
leukemia
progression is
not
yet completely understood, VEGF and its receptors may provide promising targets
not
only in solid tumors but also hematological malignancies such as
AML
.
[MeSH-minor]
Cell
Proliferation.
Cell
Survival.
Disease
Progression. Humans
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(PMID = 17305503.001).
[ISSN]
1873-5592
[Journal-full-title]
Current drug targets
[ISO-abbreviation]
Curr Drug Targets
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
[Number-of-references]
226
32.
Rickerts V, Atta J, Herrmann S, Jacobi V, Lambrecht E, Bialek R, Just-Nübling G:
Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.
Mycoses
; 2006;49 Suppl 1:27-30
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[Title]
Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with
acute
myeloid leukaemia
.
[MeSH-major]
Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
AMPHOTERICIN B
.
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(PMID = 16961579.001).
[ISSN]
0933-7407
[Journal-full-title]
Mycoses
[ISO-abbreviation]
Mycoses
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B
33.
Gill S, Olson JA, Negrin RS:
Natural killer cells in allogeneic transplantation: effect on engraftment, graft- versus-tumor, and graft-versus-host responses.
Biol Blood Marrow Transplant
; 2009 Jul;15(7):765-76
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Their response to "missing self" signals was described 3 decades ago, but the recent discovery
of a
panoply of activating receptors has made it clear that NK
cell
reactivity arises from a combination of inhibitory and activating signals.
Successful clinical exploitation of NK
cell
reactivity was demonstrated in allogeneic transplantation for
acute myelogenous leukemia
from HLA-haploidentical donors when matched donors were
not
available.
This review summarizes the heterogeneous clinical results and explains them based on a succinct description of NK
cell
biology.
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.
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.
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[Cites]
Leukemia. 2005 Aug;19(8):1446-51
[
15973456.001
]
[Cites]
Nature. 2005 Aug 4;436(7051):709-13
[
16079848.001
]
[Cites]
Nat Immunol. 2005 Sep;6(9):938-45
[
16086018.001
]
[Cites]
J Immunol. 2005 Nov 1;175(9):5966-74
[
16237090.001
]
(PMID = 19539207.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / R01 CA125276-02; United States / NCI NIH HHS / CA / CA125276-02; United States / NCI NIH HHS / CA / R01 CA125276
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Number-of-references]
139
[Other-IDs]
NLM/ NIHMS205040; NLM/ PMC2884143
34.
Cammenga J, Niebuhr B, Horn S, Bergholz U, Putz G, Buchholz F, Löhler J, Stocking C:
RUNX1 DNA-binding mutants, associated with minimally differentiated acute myelogenous leukemia, disrupt myeloid differentiation.
Cancer Res
; 2007 Jan 15;67(2):537-45
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[Title]
RUNX1 DNA-binding mutants, associated with minimally differentiated
acute myelogenous leukemia
, disrupt
myeloid
differentiation.
Mutations in the RUNX1 gene are found at high frequencies in minimally differentiated
acute myelogenous leukemia
.
Significantly, the RDB mutants did
not
act in a transdominant fashion in vivo to disrupt Runx1 activity in either T-
cell
or platelet development, which are highly sensitive to Runx1 dosage.
Disruption of the interface that binds CBFbeta, an important cofactor of Runx1, did
not
impair RDB mutant replating activity, arguing against inactivation of Runx1 function by CBFbeta sequestration.
[MeSH-major]
Cell
Differentiation / genetics. Core Binding Factor Alpha 2 Subunit / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ pathology
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(PMID = 17234761.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / RUNX1 protein, human
35.
Gong H, Liu WL, Zhou JF, Xu HZ:
[Expression of mitosis checkpoint gene CHFR in acute leukemia].
Zhonghua Yi Xue Za Zhi
; 2005 Apr 27;85(16):1085-8
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[Title]
[Expression of mitosis checkpoint gene CHFR in
acute leukemia
].
OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with
acute leukemia
(AL) and its clinical significance.
METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with
acute
myelocytic
leukemia
(
AML
) and 22 with
acute
lymphocytic
leukemia
(ALL), 45
de
novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
The
cell
cycle was examined by flow cytometric analysis.
(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent
acute
lymphoblastic
leukemia
(ALL) was 0.71, significantly higher than that of the
de
novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with
acute leukemia
.
Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of
acute leukemia
to chemotherapy.
[MeSH-major]
Cell
Cycle Proteins / biosynthesis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasm Proteins / biosynthesis. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Adult. Antineoplastic Agents / pharmacology.
Cell
Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics
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(PMID = 16029562.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
36.
Kuwayama Y, Suzuki T, Moriuchi S, Glorioso JC, Bessho M:
I kappa B-mediated apoptotic gene therapy against acute myelogenous leukemia using replication-defective HSV-1 vector expressing TK and mutant I kappa B alpha.
Cell Mol Biol (Noisy-le-grand)
; 2005;51(1):77-86
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[Title]
I kappa B-mediated apoptotic gene therapy against
acute myelogenous leukemia
using replication-defective HSV-1 vector expressing TK and mutant I kappa B alpha.
Overexpression of NF-kappa B reportedly plays anti-apoptotic roles in the growth
of AML
cells.
Control
of AML cell
growth was attempted using a replication-defective herpes simplex virus-1 vector, T0I kappa B alpha, overexpressing mutant I kappa B alpha to inhibit NF-kappa B in vitro.
Infection of T0I kappa B alpha at 15 multiplicity of infection (MOI) with cells
of AML
lines, HL60, K562, and NB4 displaying >90% infection efficiency and tumor killing in vitro.
Fresh
AML
cells from 8 patients were infected with T0I kappa B alpha at 3 MOI, with or without GCV or 10 microM of Ara-C in vitro.
Our results suggest that T0I kappa B alpha-mediated gene therapy induces apoptosis
of AML
cells in vitro.
[MeSH-major]
Apoptosis. Genetic Therapy. Herpesvirus 1, Human / genetics. I-kappa B Kinase / metabolism. I-kappa B Proteins / metabolism.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ pathology
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GANCICLOVIR
.
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(PMID = 16171566.001).
[ISSN]
1165-158X
[Journal-full-title]
Cellular and molecular biology (Noisy-le-Grand, France)
[ISO-abbreviation]
Cell. Mol. Biol. (Noisy-le-grand)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
France
[Chemical-registry-number]
0 / I-kappa B Proteins; EC 2.7.1.21 / Thymidine Kinase; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3; P9G3CKZ4P5 / Ganciclovir
37.
Zhou Q, Bucher C, Munger ME, Highfill SL, Tolar J, Munn DH, Levine BL, Riddle M, June CH, Vallera DA, Weigel BJ, Blazar BR:
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.
Blood
; 2009 Oct 29;114(18):3793-802
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[Title]
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-
cell
immunotherapy in murine
acute
myeloid
leukemia
.
To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine
acute
myeloid
leukemia
(
AML
).
AML
progression resulted in a progressive regulatory T-
cell
(Treg) accumulation in
disease
sites.
The adoptive transfer of in vitro-generated, potently lytic anti-
AML
-reactive CTLs failed to reduce
disease
burden or extend survival.
Compared with
non
-
AML
-bearing hosts, transferred CTLs had reduced proliferation in
AML
sites of metastases.
Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced
AML disease
burden but did
not
permit long-term survival.
In contrast, IL-2DT prevented anti-
AML
CTL hypoproliferation, increased the number of transferred CTLs at
AML disease
sites, reduced
AML
tumor burden, and resulted in long-term survivors that sustained an anti-
AML memory
response.
These data demonstrated that Tregs present at
AML disease
sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.
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(PMID = 19724059.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin
[Other-IDs]
NLM/ PMC2773484
38.
Löwenberg B, Delwel HR, Valk PJ:
[The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].
Ned Tijdschr Geneeskd
; 2005 Mar 19;149(12):623-5
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[Title]
[The
diagnosis of
acute
myeloid leukaemia
enhanced by using DNA microarrays].
[Transliterated title]
Diagnostiek van
acute
myeloïde
leukemie
in een stroomversnelling door toepassing van DNA-microarrays.
Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the
classification of
acute
myeloid leukaemia
(
AML
).
In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups
of AML
.
Chromosomal
lesions
, mutations, and abnormal gene expression with prognostic value determined the clustering.
In fact, gene-expression profiling recognized
leukaemias
with certain chromosomal aberrations that had been missed by routine cytogenetics.
Thus, gene-expression profiling allows a comprehensive
classification of AML
that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.
[MeSH-major]
Chromosome Aberrations. Gene Expression Profiling / methods.
Leukemia
,
Myeloid
/
diagnosis
.
Leukemia
,
Myeloid
/ genetics. Oligonucleotide Array Sequence Analysis
[MeSH-minor]
Acute
Disease
. Cluster Analysis. Cytogenetic Analysis. Humans
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[CommentIn]
Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22
[
15813427.001
]
(PMID = 15813428.001).
[ISSN]
0028-2162
[Journal-full-title]
Nederlands tijdschrift voor geneeskunde
[ISO-abbreviation]
Ned Tijdschr Geneeskd
[Language]
dut
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Netherlands
39.
Jädersten M, Montgomery SM, Dybedal I, Porwit-MacDonald A, Hellström-Lindberg E:
Long-term outcome of treatment of anemia in MDS with erythropoietin and G-CSF.
Blood
; 2005 Aug 1;106(3):803-11
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The
International
Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).
The time until 25% developed
acute
myeloid
leukemia
(
AML
) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).
Only 1 of 20 long-term responders developed
AML
.
There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk
of AML
evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.
Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should
not
be considered candidates for this treatment.
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance.
Cell
Transformation, Neoplastic. Female. Humans.
Leukemia
,
Myeloid
/ etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome
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(PMID = 15840690.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor
40.
van der Straaten HM, Fijnheer R, Nieuwenhuis HK, van de Winkel JG, Verdonck LF:
The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.
Biol Blood Marrow Transplant
; 2005 Mar;11(3):206-12
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[Title]
The FcgammaRIIa-polymorphic site as a potential target for
acute
graft-versus-host
disease
in allogeneic stem
cell
transplantation.
Graft-versus-host
disease
(GVHD) is a serious complication of allogeneic stem
cell
transplantation for hematologic
diseases
.
Polymorphisms are known for FcgammaRIIa, and this
molecule
is present on endothelial, dendritic, and Langerhans cells.
Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-
leukemia
(GVL) effect.
Because the FcgammaRIIa
molecule
is also present on
acute
myeloid
leukemia
(
AML
) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.
We retrospectively studied 73
AML
patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.
Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of
acute
GVHD.
The relapse incidence was
not
significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk
AML
patients with the pro-GVL mismatch.
We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for
acute
GVHD.
[MeSH-major]
Antigens, CD / genetics. Graft vs Host
Disease
/ genetics. Hematopoietic Stem
Cell
Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics
[MeSH-minor]
Acute
Disease
. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs
Leukemia
Effect / genetics. Graft vs
Leukemia
Effect / immunology. Humans. Incidence.
Leukemia
,
Myeloid
/ complications.
Leukemia
,
Myeloid
/ therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous
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(PMID = 15744239.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG
41.
Dheda K, Davids V, Lenders L, Roberts T, Meldau R, Ling D, Brunet L, van Zyl Smit R, Peter J, Green C, Badri M, Sechi L, Sharma S, Hoelscher M, Dawson R, Whitelaw A, Blackburn J, Pai M, Zumla A:
Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.
PLoS One
; 2010 Mar 24;5(3):e9848
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[Title]
Clinical utility
of a
commercial
LAM
-ELISA assay for TB
diagnosis
in HIV-infected patients using urine and sputum samples.
BACKGROUND: The accurate
diagnosis of
TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.
Recent studies indicate that a lipoarabinomannan (
LAM
) assay (Clearview-TB(R)-ELISA) may have some utility for the
diagnosis of
TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.
The utility
of LAM
in sputum samples has, hitherto,
not
been evaluated.
METHODS:
LAM
was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.
Culture positivity
for M
. tuberculosis was used as the reference standard for TB
diagnosis
.
Urine-
LAM
positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).
Urine-
LAM
remained highly specific in all 3 subgroups (95%-100%).
25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-
LAM
.
Sputum-
LAM
had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.
CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-
LAM
is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would
otherwise
have required further investigation.
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.
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consumer health - HIV/AIDS
.
MedlinePlus Health Information.
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.
MedlinePlus Health Information.
consumer health - Tuberculosis
.
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[Cites]
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]
[Cites]
J Microbiol Methods. 2001 May;45(1):41-52
[
11295196.001
]
(PMID = 20352098.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
ENG
[Grant]
None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2844421
42.
Paschka P:
Core binding factor acute myeloid leukemia.
Semin Oncol
; 2008 Aug;35(4):410-7
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[Title]
Core binding factor
acute
myeloid
leukemia
.
Core binding factor (CBF)
acute
myeloid
leukemia
(
AML
) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult
de
novo
AML
cases.
Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16)
AML
, thereby supporting the notion that they represent two distinct biologic and clinical entities.
Furthermore, despite being considered as a more favorable
AML
risk group, only approximately half of the CBF
AML
patients are cured with current therapy, indicating the need for improved therapeutic approaches.
This review summarizes the most recent laboratory and clinical discoveries relevant to this subset
of AML
and how they are being applied for in an effort to improve the cure rate in patients with the
disease
.
[MeSH-major]
Chromosome Inversion. Core Binding Factors / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy. Translocation, Genetic
[MeSH-minor]
Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual /
diagnosis
. Prognosis
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.
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.
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(PMID = 18692691.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors
[Number-of-references]
76
43.
Shim H, Chi HS, Jang S, Seo EJ, Park CJ, Lee JH, Lee JH, Lee KH:
Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
Korean J Hematol
; 2010 Sep;45(3):177-82
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[Title]
Therapy-related
acute leukemia
in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
BACKGROUND: Therapy-related
myeloid
neoplasm (t-MN) is a distinct class of
acute
myeloid
leukemia
(
AML
) in the World Health Organization (WHO)
classification
.
Both
AML
and
acute
lymphoblastic
leukemia
(ALL) may develop after treatment for primary cancer.
Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related
acute
leukemias
(t-AL).
METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed
acute leukemia
.
Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related
AML
(t-
AML
) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).
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[Cites]
J Clin Oncol. 2003 Apr 1;21(7):1195-204
[
12663705.001
]
[Cites]
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16037905.001
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]
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]
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]
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]
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]
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[
15378478.001
]
[Cites]
Br J Haematol. 1999 Sep;106(4):1037-40
[
10520009.001
]
(PMID = 21120206.001).
[ISSN]
2092-9129
[Journal-full-title]
The Korean journal of hematology
[ISO-abbreviation]
Korean J Hematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2983048
[Keywords]
NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors
44.
Edwards DB, Tempelman RJ, Bates RO:
Evaluation of Duroc- vs. Pietrain-sired pigs for growth and composition.
J Anim Sci
; 2006 Feb;84(2):266-75
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Body weight, 10th rib backfat (BF10), last rib backfat (LRF), and loin muscle
area
(
LMA
) were serially measured at 10, 13, 16, 19, 22, 24, and 26 wk of age.
At 26 wk of age, Duroc-sired progeny were heavier (143.4 vs. 132.7 kg, P < 0.001), had more BF10 (27.1 vs. 23.7 mm, P < 0.001) and LRF (21.2 vs. 19.2 mm, P < 0.001), but had similar
LMA
(46.4 vs. 47.1 cm2) compared with Pietrain-sired progeny.
Mean feed efficiency did
not
differ between breed of sire in any period of the study.
Random regression animal models with polynomial regression on week on-test were fitted to BW, BF10, LRF,
LMA
, FFTOLN, TOFAT, EBPRO, and EBLIPID from 10 to 26 wk of age.
Serial heritability estimates generally increased from 10 to 26 wk of age with ranges as follows: BW (0.05 to 0.39), BF10 (0.13 to 0.76), LRF (0.11 to 0.79),
LMA
(0.05 to 0.73), FFTOLN (0.07 to 0.16), TOFAT (0.19 to 0.45), EBPRO (0.02 to 0.55), and EBLIPID (0.12 to 0.60).
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(PMID = 16424252.001).
[ISSN]
1525-3163
[Journal-full-title]
Journal of animal science
[ISO-abbreviation]
J. Anim. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
45.
Song KY, Kang WK, Park CW, Choi YJ, Rha SE, Park CH:
Mucormycosis resulting in gastric perforation in a patient with acute myelogenous leukemia: report of a case.
Surg Today
; 2006;36(9):831-4
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[Title]
Mucormycosis resulting in gastric perforation in a patient with
acute myelogenous leukemia
: report
of a
case.
Mucormycosis is an uncommon opportunistic fungal infection that may develop in immunocompromised patients with conditions such as diabetes mellitus,
leukemia
, lymphoma, or human immunodeficiency virus (HIV), or after transplantation with immunosupperessive therapy.
We report a case of gastric perforation caused by a mucormycosis infection in a patient with
acute myelogenous leukemia
(
AML
).
[MeSH-major]
Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Gastrectomy. Intestinal Perforation / etiology.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Mucormycosis / complications. Stomach / injuries. Treatment Outcome
Genetic Alliance.
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.
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.
Hazardous Substances Data Bank.
AMPHOTERICIN B
.
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[Cites]
Am J Gastroenterol. 1979 Oct;72 (4):379-94
[
517498.001
]
[Cites]
Surg Today. 2003;33(4):319-22
[
12707834.001
]
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[
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]
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]
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Pharmacotherapy. 2002 Apr;22(4):519-26
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]
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[
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]
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[
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]
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Rev Infect Dis. 1989 Sep-Oct;11(5):741-54
[
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[
3951358.001
]
[Cites]
Drugs. 2004;64(18):1997-2020
[
15341494.001
]
(PMID = 16937290.001).
[ISSN]
0941-1291
[Journal-full-title]
Surgery today
[ISO-abbreviation]
Surg. Today
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
46.
Nahimana A, Attinger A, Aubry D, Greaney P, Ireson C, Thougaard AV, Tjørnelund J, Dawson KM, Dupuis M, Duchosal MA:
The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies.
Blood
; 2009 Apr 2;113(14):3276-86
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Intracellular NAD is essential
for cell
survival, and NAD depletion resulting from APO866 treatment elicits tumor
cell
death.
Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel
of cell
lines (n = 45) and primary cells (n = 32).
Most cancer cells (
acute
myeloid
leukemia
[
AML
],
acute
lymphoblastic
leukemia
[ALL], mantle
cell
lymphoma [MCL], chronic
lymphocytic
leukemia
[CLL], and T-
cell
lymphoma), but
not
normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.
The NAD depletion led to
cell
death.
At 96 hours, APO866-mediated
cell
death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.
Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human
AML
,
lymphoblastic
lymphoma, and
leukemia
without significant toxicity to the animals.
[MeSH-minor]
Animals.
Cell
Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays
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[CommentIn]
Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8
[
19498032.001
]
(PMID = 19196867.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
47.
Chowdhury T, Brady HJ:
Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
Blood Cells Mol Dis
; 2008 Mar-Apr;40(2):192-9
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[Title]
Insights from clinical studies into the role of the MLL gene in infant and childhood
leukemia
.
Translocations involving the Mixed Lineage
Leukemia
(MLL) gene at 11q23 are found in both
acute
lymphoblastic
leukemia
(ALL) and
acute
myeloblastic
leukemia
(
AML
), but have different prognostic implications depending on the phenotype of the
leukemia
in
de
novo pediatric cases.
Rearrangements of the MLL gene are found in most cases of infant
AML
and regardless of age confer an intermediate risk.
The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and
AML
-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.
The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged
leukemias
is shedding light on the molecular mechanisms and potential therapeutic targets of these
leukemias
.
It may also prove to have a useful role in both
diagnosis
and prognosis.
[MeSH-major]
Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
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(PMID = 17905612.001).
[ISSN]
1079-9796
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Number-of-references]
82
48.
Czibere A, Grall F, Aivado M:
Perspectives of proteomics in acute myeloid leukemia.
Expert Rev Anticancer Ther
; 2006 Nov;6(11):1663-75
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[Title]
Perspectives of proteomics in
acute
myeloid
leukemia
.
Acute
myeloid
leukemia
(
AML
) is a frequent hematological malignancy.
Despite enormous therapeutic efforts that range from various cytotoxic agents to allogeneic stem
cell
transplantation, overall survival of patients with
AML
remains unsatisfying.
There is hope that elucidation of the
AML
-specific proteome will prompt the discovery of novel therapeutic targets and biomarkers in
AML
.
Modern mass-spectrometry instrumentation has achieved excellent performance in terms of sensitivity, resolution and mass accuracy; however, so far, the contribution of proteomics to the care of patients with
AML
is virtually zero.
Since mass-spectrometry instruments are very intricate devices, their successful operation will hinge on the willingness and ability of mass-spectrometry experts and clinical researchers to adopt new views, learn from each other and cooperate in order to ultimately benefit the patient suffering from
AML
.
This review highlights some clinical problems circumventing the treatment of patients with
AML
.
Furthermore, it provides a brief overview of the technical background of standard proteomics approaches and describes opportunities, challenges and pitfalls of proteomic studies with regards to
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy. Proteomics
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(PMID = 17134369.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
[Number-of-references]
99
49.
Schlenk RF, Döhner K, Kneba M, Götze K, Hartmann F, Del Valle F, Kirchen H, Koller E, Fischer JT, Bullinger L, Habdank M, Späth D, Groner S, Krebs B, Kayser S, Corbacioglu A, Anhalt A, Benner A, Fröhling S, Döhner H, German-Austrian AML Study Group (AMLSG):
Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B.
Haematologica
; 2009 Jan;94(1):54-60
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[Title]
Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with
acute
myeloid
leukemia
. Results from the AMLSG Trial
AML
HD98B.
BACKGROUND: In a previous randomized trial,
AML
HD98B, we showed that administration of all-trans retinoic acid in addition to intensive chemotherapy improved the outcome of older patients with
acute
myeloid
leukemia
.
DESIGN AND METHODS: Data from mutation analyses of the NPM1, CEBPA, FLT3, and MLL genes were correlated with outcome in patients 61 years and older treated within the
AML
HD98B trial.
The genotype mutant NPM1 was positively and adverse cytogenetics as well as higher white blood
cell
count negatively correlated with achievement of complete remission.
Other significant factors for survival were age, adverse cytogenetics, and logarithm of white
cell
count.
CONCLUSIONS: In elderly patients with
acute
myeloid
leukemia
, NPM1 mutations are associated with achievement of complete remission, and the genotype 'mutant NPM1 without FLT3-ITD' appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242).
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation / genetics. Tretinoin / therapeutic use
[MeSH-minor]
Aged. Aged, 80 and over. Biomarkers / metabolism.
Disease
-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Survival Rate. Treatment Outcome
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.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
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NCI CPTAC Assay Portal
.
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Cited by Patents in
.
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[Cites]
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]
[CommentIn]
Haematologica. 2009 Jan;94(1):10-6
[
19118375.001
]
(PMID = 19059939.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00151242
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Biomarkers; 5688UTC01R / Tretinoin
[Other-IDs]
NLM/ PMC2625424
[Investigator]
Glasmacher A; Mergenthaler HG; Nerl C; Pralle H; Hensel M; Preiss J; Salwender H; Biedermann HG; Kremers S; Griesinger F
50.
Jenkins CI, Sorour Y:
Case report: A large extramedullary granulocytic sarcoma as the initial presenting feature of chronic myeloid leukemia.
MedGenMed
; 2005;7(4):23
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[Title]
Case report: A large extramedullary
granulocytic
sarcoma as the initial presenting feature of chronic
myeloid
leukemia
.
Granulocytic
sarcomas (chloromas) are rare extramedullary tumors consisting of primitive
granulocytic
cells.
They arise
de
novo, or are associated with other hematologic disorders such as
acute
myeloid
leukemia
, myelodysplastic syndrome, or myeloproliferative disorders.
We report here on a case
of a
62-year-old woman who presented with a large swelling in her right groin and leg.
The mass was confirmed by biopsy to be
a granulocytic
sarcoma.
However, cytogenetic examination of the marrow showed t(9;22), indicating an unexpected
diagnosis of
chronic
myeloid
leukemia
.
[MeSH-major]
Bone Marrow Neoplasms / complications. Bone Marrow Neoplasms / pathology. Edema / etiology.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / complications.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / pathology. Sarcoma,
Myeloid
/ complications. Sarcoma,
Myeloid
/ pathology
[MeSH-minor]
Chronic
Disease
.
Diagnosis
, Differential. Female. Groin / pathology. Humans. Leg / pathology. Middle Aged. Rare
Diseases
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.
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.
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[Cites]
Ann Hematol. 2002 Feb;81(2):108-10
[
11907793.001
]
[Cites]
Leuk Lymphoma. 1994 Oct;15(3-4):351-5
[
7866286.001
]
[Cites]
Ann Intern Med. 1995 Sep 1;123(5):351-3
[
7625623.001
]
[Cites]
J Clin Neurosci. 2004 Nov;11(8):914-7
[
15519878.001
]
(PMID = 16614645.001).
[ISSN]
1531-0132
[Journal-full-title]
MedGenMed : Medscape general medicine
[ISO-abbreviation]
MedGenMed
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1681710
51.
Griessinger E, Imbert V, Lagadec P, Gonthier N, Dubreuil P, Romanelli A, Dreano M, Peyron JF:
AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cells.
Leukemia
; 2007 May;21(5):877-85
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[Title]
AS602868, a dual inhibitor of IKK2 and FLT3 to target
AML
cells.
Acute
myeloid
leukemia
(
AML
) cells carry molecular defects that promote their leukemic proliferation, resistance to apoptosis and defect in differentiation.
Pharmacological targeting of the nuclear factor kappaB (NF-kappaB) pathway has been shown to promote apoptosis of primary
AML
cells and to sensitize blasts to neoplastic drugs (Frelin, Blood 2005, 105, 804).
The Fms-like tyrosine kinase 3 (FLT3), which sustains proliferation of normal hematopoietic progenitors is frequently overexpressed or mutated in
AML
patients.
Using Ba/F3 murine pre-B cells transfected with various mutants of FLT3 (ITD, D835V, D835Y) and the MV4-11 human
AML
line, we show that normal or oncogenic stimulation of FLT3 led to activation of NF-kappaB.
Pharmacological inhibition of either FLT3 with AG1296 or NF-kappaB with the small
molecule
inhibitor of IkappaB kinase-2 AS602868 reduced viability and triggered
cell
death.
AS602868 thus appears to target two different kinases that play a crucial role in the pathogenesis
of AML
, making it particularly attractive as a new therapeutical approach
for AML
.
[MeSH-major]
I-kappa B Kinase / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
[MeSH-minor]
Animals. Annexin A5 / analysis. Caspase 3 / metabolism.
Cell
Line.
Cell
Proliferation. Child. Humans. Male. Mice. NF-kappa B / metabolism. Poly(ADP-ribose) Polymerases / metabolism. bcl-X Protein / analysis
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(PMID = 17330097.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / AS602868; 0 / Annexin A5; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / bcl-X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3
52.
Siegler U, Meyer-Monard S, Jörger S, Stern M, Tichelli A, Gratwohl A, Wodnar-Filipowicz A, Kalberer CP:
Good manufacturing practice-compliant cell sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to leukemia patients.
Cytotherapy
; 2010 Oct;12(6):750-63
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[Title]
Good manufacturing practice-compliant
cell
sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to
leukemia
patients.
The introduction of NK
cell
-based immunotherapy to current treatment options in
acute
myeloid
leukemia
(
AML
) requires NK
cell
products with high anti-leukemic efficacy optimized for clinical use.
METHODS: We describe a good manufacturing practice (GMP)-compliant protocol of large-scale ex vivo expansion of alloreactive NK cells suitable for multiple donor
lymphocyte
infusions (NK-DLI) in
AML
.
NK
cell
numbers increased 117.0 ± 20.0-fold in 19 days.
To reduce the culture volume associated with expansion of bulk NK cells and to expand selectively the alloreactive NK
cell
subsets, GMP-certified
cell
sorting was introduced to obtain cells with single killer immunoglobulin-like receptor (KIR) specificities.
The subsequent GMP-compliant expansion of single KIR+ cells was 268.3 ± 66.8-fold, with a contaminating T-
cell
content of only 0.006 ± 0.002%.
The single KIR-expressing NK cells were cytotoxic against HLA-mismatched primary
AML
blasts in vitro and effectively reduced tumor
cell
load in vivo in NOD/SCID mice transplanted with human
AML
.
CONCLUSIONS: The approach to generating large numbers of GMP-grade alloreactive NK cells described here provides the basis for clinical efficacy trials of NK-DLI to complement and advance therapeutic strategies against human
AML
.
[MeSH-major]
Cell
Culture Techniques / methods.
Cell
Proliferation. Immunotherapy, Adoptive. Killer Cells, Natural / metabolism.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Animals. Antineoplastic Protocols.
Cell
Line, Tumor. Cytotoxicity, Immunologic. Guideline Adherence. Humans. Infusions, Intravenous. Isoantigens / immunology. Mice. Mice, SCID. Neoplasm Transplantation. Receptors, KIR / metabolism. Tumor Burden
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(PMID = 20491532.001).
[ISSN]
1477-2566
[Journal-full-title]
Cytotherapy
[ISO-abbreviation]
Cytotherapy
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Isoantigens; 0 / Receptors, KIR
53.
Liu XM, Chen YZ, Huang MJ, Liu X, Guo JR:
[The potential prognostic influence of granulocyte-colony stimulating factor in acute leukemia].
Zhonghua Nei Ke Za Zhi
; 2005 Jul;44(7):518-21
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[Title]
[The potential prognostic influence of granulocyte-colony stimulating factor in
acute leukemia
].
OBJECTIVE: To investigate the potential influence of granulocyte-colony stimulating factor (G-CSF) on the prognosis of patients with
acute leukemia
(AL).
METHODS: In 171 evaluable cases with AL, the complete remission (CR) rate post first course of chemotherapy, CR rate, effective rate, duration of leucopenia post chemotherapy, CR duration, lifespan and the relationship between the dosage
of G
-CSF and CR duration or lifespan were retrospectively analyzed with Chi-square test, paired t-test, Cox regression, Kaplan-Meier and rank correlation method.
For remission induction and postremission therapy, the cases with
acute
myeloid
leukemia
(
AML
) received chemotherapy regimes based on daunorubicin + ara-C (DA), homoharringtonine + ara-C (HA) or mitoxantrone + ara-C (MA).
The patients with
acute
lymphocyte
leukemia
(ALL) were treated with regimes based on vinblastine + daunorubicin + prednisone (VDP), vinblastine + adriamycin + prednisone (VAP), vinblastine + mitoxantrone + prednisone (VMP) or cyclophosphamide + vinblastine + daunorubicin + prednisone(CODP).
However, there was no statistical difference between the two groups in the CR rate post first course of chemotherapy, CR rate and the effective rate of treatment. (2) Use
of G
-CSF did
not
affect CR durations of ALL patients, but shortened that
of AML
patients. (3) The application
of G
-CSF had little effect on the lifespan of ALL patients.
By contrast, it showed clearly negative effects on that
of AML
patients. (4) No relationship between the dosage
of G
-CSF and CR duration or lifespan in
AML
patients.
CONCLUSION: With
AML
patients, the administration
of G
-CSF must be very cautious.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulocyte Colony-Stimulating Factor / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy
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(PMID = 16080844.001).
[ISSN]
0578-1426
[Journal-full-title]
Zhonghua nei ke za zhi
[ISO-abbreviation]
Zhonghua Nei Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
143011-72-7 / Granulocyte Colony-Stimulating Factor
54.
Cilloni D, Messa E, Messa F, Carturan S, Defilippi I, Arruga F, Rosso V, Catalano R, Bracco E, Nicoli P, Saglio G:
Genetic abnormalities as targets for molecular therapies in myelodysplastic syndromes.
Ann N Y Acad Sci
; 2006 Nov;1089:411-23
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Recent advances in molecular genetics have increased knowledge regarding the mechanisms leading to myelodysplastic syndrome (MDS), secondary
acute
myeloid
leukemia
(
AML
), and therapy-induced MDS.
Many genetic defects underlying MDS and
AML
have been identified thereby allowing the development of new molecular-targeted therapies.
These agents have been tested in patients with solid tumors and hematologic malignancies such as
AML
and MDS.
The DNA hypomethylating compounds azacytidine and decitabine may reduce hypermethylation and induce
re
-expression of key tumor suppressor genes in MDS.
Future therapies will attempt to resolve cytopenias in MDS, eliminate malignant clones, and allow differentiation by attacking specific mechanisms of the
disease
.
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(PMID = 17261784.001).
[ISSN]
0077-8923
[Journal-full-title]
Annals of the New York Academy of Sciences
[ISO-abbreviation]
Ann. N. Y. Acad. Sci.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MECOM protein, human; 0 / Transcription Factors; 0 / WT1 Proteins; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
[Number-of-references]
76
55.
Lösler S, Schlief S, Kneifel C, Thiel E, Schrezenmeier H, Rojewski MT:
Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic cell lines, recruitment of caspases, and loss of mitochondrial membrane potential are enhanced by modulators of the cellular glutathione redox system.
Ann Hematol
; 2009 Nov;88(11):1047-58
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[Title]
Antimony-trioxide- and arsenic-trioxide-induced apoptosis in myelogenic and lymphatic
cell
lines, recruitment of caspases, and loss of mitochondrial
membrane
potential are enhanced by modulators of the cellular glutathione redox system.
During the last years remission rates of more than 72% for arsenic(III)-oxide (As(2)O(3)) treatment in relapsed or refractory
acute
promyelocytic
leukemia
have been published.
As(2)O(3) is under clinical investigation for therapy of
leukemia
and solid tumors.
Based on the same molar concentrations, lower efficacy in apoptosis induction and caspase-independent decrease of mitochondrial
membrane
potential was observed for Sb(2)O(3).
Other modulators of the cellular redox system showed this effect to a lower extent and enhancement was
not
consistent for the different
cell
lines tested.
Caspase inhibitors protected
cell
lines from Sb(2)O(3)- and As(2)O(3)-induced apoptosis.
[MeSH-major]
Antimony / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Arsenicals / pharmacology. Glutathione / physiology.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / pathology.
Leukemia
, T-
Cell
/ pathology. Oxides / pharmacology
[MeSH-minor]
Buthionine Sulfoximine / pharmacology. Caspase Inhibitors. Caspases / metabolism.
Cell
Line, Tumor / cytology.
Cell
Line, Tumor / drug effects.
Cell
Line, Tumor / enzymology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Drug Synergism. HL-60 Cells / cytology. HL-60 Cells / drug effects. HL-60 Cells / enzymology. Humans. K562 Cells / cytology. K562 Cells / drug effects. K562 Cells / enzymology.
Membrane
Potential, Mitochondrial / drug effects. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Proteins / metabolism. Oxidation-Reduction
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.
Hazardous Substances Data Bank.
ANTIMONY TRIOXIDE
.
Hazardous Substances Data Bank.
ARSENIC TRIOXIDE
.
Hazardous Substances Data Bank.
ANTIMONY, ELEMENTAL
.
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(PMID = 19301004.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Caspase Inhibitors; 0 / Neoplasm Proteins; 0 / Oxides; 5072-26-4 / Buthionine Sulfoximine; 9IT35J3UV3 / Antimony; EC 3.4.22.- / Caspases; GAN16C9B8O / Glutathione; P217481X5E / antimony trioxide; S7V92P67HO / arsenic trioxide
56.
Pan J, Zou J, Wu DY, Roberson RS, Hennings LJ, Ma X, Yared M, Blackburn ML, Chansky HA, Yang L:
TLS-ERG leukemia fusion protein deregulates cyclin-dependent kinase 1 and blocks terminal differentiation of myeloid progenitor cells.
Mol Cancer Res
; 2008 May;6(5):862-72
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[Title]
TLS-ERG
leukemia
fusion protein deregulates cyclin-dependent kinase 1 and blocks terminal differentiation
of myeloid
progenitor cells.
TLS-ERG fusion protein is derived from the t(16;21) translocation found in human
myeloid
leukemia
.
Here, we show that retroviral transduction of TLS-ERG confers a growth advantage to L-
G myeloid
progenitor cells and blocks terminal differentiation.
Injection of TLS-ERG-expressing L-G cells induced rapid development
of a
leukemia
-like
disease
in syngeneic mice.
In addition, siRNA knockdown of Cdk1 in YNH-1 cells derived from a t(16;21)
acute myelogenous leukemia
patient also resulted in terminal differentiation.
As restoration of terminal
myeloid
differentiation to TLS-ERG cells is dependent on
cell
cycle arrest, our findings suggest an important role for Cdk1 in cellular transformation and may be useful in the search for new treatments of TLS-ERG-associated
myeloid
leukemia
.
[MeSH-major]
Myeloid
Progenitor Cells / cytology. Oncogene Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Protein c-ets-1 / metabolism. RNA-Binding Protein FUS / metabolism
[MeSH-minor]
Animals. Antimetabolites, Antineoplastic / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. CDC2 Protein Kinase / metabolism.
Cell
Differentiation. Epigenesis, Genetic. Granulocyte Colony-Stimulating Factor / metabolism. Hydroxamic Acids / pharmacology. Interleukin-3 / metabolism. Mice. Protein Structure, Tertiary. Protein Synthesis Inhibitors / pharmacology. Transcription Factors
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(PMID = 18505930.001).
[ISSN]
1541-7786
[Journal-full-title]
Molecular cancer research : MCR
[ISO-abbreviation]
Mol. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA090941
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / ERG protein, mouse; 0 / Hydroxamic Acids; 0 / Interleukin-3; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Synthesis Inhibitors; 0 / Proto-Oncogene Protein c-ets-1; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, mouse; 0 / Transcription Factors; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.7.11.22 / CDC2 Protein Kinase; M801H13NRU / Azacitidine
57.
Yang L, Dong ZR, Wen SP, Pan L, Zhang XJ, Luo JM, Xu SR:
[Relationship between VEGF and MMP-2, MMP-9 in 82 patients with acute myeloid leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2006 Feb;14(1):15-20
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[Title]
[Relationship between VEGF and MMP-2, MMP-9 in 82 patients with
acute
myeloid
leukemia
].
In order to investigate the relationship between VEGF and matrix metalloproteinase (MMP)-2, -9 in
acute
myeloid
leukemia
patients, and evaluate the significance of them in extramedullary leukemic invasion, the expressions of MMP-2 mRNA, MMP-9 mRNA, VEGF mRNA in bone marrow from 86 patients with
acute
myeloid
leukemia
(
AML
), as well as human hematopoietic
cell
lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR).
But no such correlation was demonstrated in the
AML
(CR) and normal control (NC) groups.
More extramedullary infiltration occurred in VEGF positive groups than that in VEGF negative groups
of AML
.
It is concluded that there are significantly positive correlations between the expression of MMP-2 and MMP-9 with VEGF mRNA or protein levels in
AML
patients.
VEGF and MMP-2, MMP-9 may participate in the extramedullary leukemic invasion
of AML
patients.
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(PMID = 16584583.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
58.
Racay P, Hatok J, Hudecek J, Chudej J, Jurecekova J, Dobrota D:
Transcription of genes of p53-dependent apoptosis in acute leukaemia.
Int J Mol Med
; 2008 Dec;22(6):833-9
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[Title]
Transcription of genes of p53-dependent apoptosis in
acute
leukaemia
.
We demonstrated that
acute
leukaemia
,
myeloblastic
(
AML
) and
lymphoblastic
(ALL), is associated with significantly elevated levels of p53 and Bax mRNA in leukaemic cells.
Altered alternative processing of Bcl-x and
myeloid cell leukaemia
-1 (MCL1) primary transcripts were observed in the case
of AML
and
AML
and ALL, respectively.
We assumed that increased glyceraldehyde-3-phosphate dehydrogenase (gapdh) transcription and decreased MCL1s mRNA were
not
fully responsible for the dysregulation of p53-dependent apoptosis in the case
of AML
.
In addition, transcription of hsp70.1 and Bcl-2 producing anti-apoptotic proteins was
not
affected in
acute
leukaemia
.
[MeSH-major]
Apoptosis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Transcription, Genetic. Tumor Suppressor Protein p53 / genetics
[MeSH-minor]
Actins / genetics. Actins / metabolism. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. HSP70 Heat-Shock Proteins / genetics. HSP70 Heat-Shock Proteins / metabolism. Humans. Leukocytes, Mononuclear / metabolism.
Myeloid Cell
Leukemia
Sequence 1 Protein. Polymorphism, Single-Stranded Conformational. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism. bcl-X Protein / genetics. bcl-X Protein / metabolism
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(PMID = 19020783.001).
[ISSN]
1107-3756
[Journal-full-title]
International journal of molecular medicine
[ISO-abbreviation]
Int. J. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Actins; 0 / BCL2L1 protein, human; 0 / HSP70 Heat-Shock Proteins; 0 / MCL1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
59.
Crapanzano JP:
Fine-needle aspiration of renal angiomyolipoma: cytological findings and diagnostic pitfalls in a series of five cases.
Diagn Cytopathol
; 2005 Jan;32(1):53-7
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Diagnosis of
renal angiomyolipoma (
AML
) by fine-needle aspiration (FNA) may be difficult because cytological and radiological findings sometimes overlap with renal
cell
carcinoma (RCC) and liposarcoma.
Five FNAs
of AMLs
were studied.
Corresponding surgical material showed typical features
of AML
.
In FNA, bland chromatin and inconspicuous nucleoli distinguish renal
AML
from RCC and liposarcoma.
Adipose tissue is
not
universally present.
Immunocytochemical (ICC) stains may elucidate the correct
diagnosis
.
[MeSH-minor]
Adenoma, Oxyphilic /
diagnosis
. Adult. Aged. Carcinoma, Renal
Cell
/
diagnosis
.
Diagnosis
, Differential. Epithelioid Cells / pathology. Female. Humans. Liposarcoma /
diagnosis
. Male. Middle Aged. Retroperitoneal Neoplasms /
diagnosis
. Stromal Cells / pathology
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 15584043.001).
[ISSN]
8755-1039
[Journal-full-title]
Diagnostic cytopathology
[ISO-abbreviation]
Diagn. Cytopathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
60.
Bhally HS, Lema C, Romagnoli M, Borek A, Wakefield T, Carroll KC:
Leptotrichia buccalis bacteremia in two patients with acute myelogenous leukemia.
Anaerobe
; 2005 Dec;11(6):350-3
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[Title]
Leptotrichia buccalis bacteremia in two patients with
acute myelogenous leukemia
.
Leptotrichia buccalis is rarely implicated in systemic
disease
.
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(PMID = 16701598.001).
[ISSN]
1075-9964
[Journal-full-title]
Anaerobe
[ISO-abbreviation]
Anaerobe
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
61.
Wang Z, Xu HX, Xie XY, Xie XH, Kuang M, Xu ZF, Liu GJ, Chen LD, Lin MX, Lu MD:
Imaging features of hepatic angiomyolipomas on real-time contrast-enhanced ultrasound.
Br J Radiol
; 2010 May;83(989):411-8
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The aim of this study was to evaluate the imaging features of hepatic angiomyolipoma (
AML
) on contrast-enhanced ultrasound (CEUS).
The imaging features of 12 pathologically proven hepatic
AML lesions
in 10 patients who had undergone baseline ultrasound (BUS) and CEUS examinations were evaluated retrospectively.
The results showed that 75% (9/12) of the
AML lesions
exhibited mixed echogenicity on BUS and most showed remarkable hyperechogenicity in combination with a hypoechoic or anechoic portion.
Arterial flow signals were detected in 75% (9/12) of the
lesions
on colour Doppler imaging.
On CEUS, 66.7% (n = 8) of the 12
lesions
exhibited hyperenhancement in the arterial phase, slight hyperenhancement (n = 2) or isoenhancement (n = 6) in the portal phase, and slight hyperenhancement (n = 1) or isoenhancement (n = 7) in the late phase.
Three (25%)
lesions
exhibited hyperenhancement in the arterial phase and hypoenhancement in both portal and late phases.
One (8.3%)
lesion
exhibited hypoenhancement throughout the CEUS process.
Before pathological examination with BUS, only 3 (25%)
lesions
were correctly diagnosed as hepatic
AML
.
Conversely, on CEUS, correct diagnoses were made for 66.8% (8/12) of hepatic
AMLs
.
Therefore, arterial hyperenhancement and subsequent sustained enhancement on CEUS were found in the majority of hepatic
AMLs
.
The combination of BUS and CEUS leads to the correct
diagnosis
in the majority of hepatic
AMLs
, and is higher than the success rate achieved by BUS alone.
[MeSH-major]
Angiomyolipoma / ultrasonography.
Liver
Neoplasms / ultrasonography
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1748-880X
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The British journal of radiology
[ISO-abbreviation]
Br J Radiol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
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England
[Chemical-registry-number]
0 / Contrast Media
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NLM/ PMC3473573
62.
Fernandes MS, Reddy MM, Croteau NJ, Walz C, Weisbach H, Podar K, Band H, Carroll M, Reiter A, Larson RA, Salgia R, Griffin JD, Sattler M:
Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism.
J Biol Chem
; 2010 Oct 15;285(42):32596-605
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[Title]
Novel oncogenic mutations of CBL in human
acute
myeloid
leukemia
that activate growth and survival pathways depend on increased metabolism.
Acute
myeloid
leukemia
(
AML
) is characterized by multiple mutagenic events that affect proliferation, survival, as well as differentiation.
Recently, gain-of-function mutations in the α helical structure within the linker sequence of the E3 ubiquitin ligase CBL have been associated with
AML
.
We identified four novel CBL mutations, including a point mutation (Y371H) and a putative splice site mutation in
AML
specimens.
Overall, our data demonstrate that mutations of CBL alter cellular biology at multiple levels and require
not
only the activation of receptor proximal signaling events but also an increase in cellular glucose metabolism.
Pathways that are activated by CBL gain-of-function mutations can be efficiently targeted by small
molecule
drugs.
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.
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.
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.
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[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA087986; United States / NCI NIH HHS / CA / 5R01CA134660-02; United States / NCI NIH HHS / CA / CA099163-11; United States / NCI NIH HHS / CA / 5R01CA87986-12; United States / NCI NIH HHS / CA / R01 CA099163-09; United States / NCI NIH HHS / CA / 5R01CA105489-06; United States / NCI NIH HHS / CA / CA099163-10; United States / NCI NIH HHS / CA / 5R01CA125541-04; United States / NCI NIH HHS / CA / 5R01CA129501-02; United States / NCI NIH HHS / CA / R01 CA125541; United States / NCI NIH HHS / CA / 5R01CA116552-04; United States / NCI NIH HHS / CA / R01 CA116552; United States / NCI NIH HHS / CA / CA099163-09; United States / NCI NIH HHS / CA / R01 CA105489; United States / NCI NIH HHS / CA / 5R01CA99163-09; United States / NCI NIH HHS / CA / R01 CA099163-11; United States / NCI NIH HHS / CA / 5R01CA100750-06; United States / NCI NIH HHS / CA / R01 CA129501; United States / NCI NIH HHS / CA / R01 CA099163-10; United States / NCI NIH HHS / CA / R01 CA061593; United States / NCI NIH HHS / CA / R01 CA099163; United States / NCI NIH HHS / CA / R01 CA100750; United States / NCI NIH HHS / CA / R01 CA134660
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / STAT5 Transcription Factor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.1.- / GTP-Binding Proteins; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; IY9XDZ35W2 / Glucose
[Other-IDs]
NLM/ PMC2952262
63.
Ngo N, Lampert IA, Naresh KN:
Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia.
Br J Haematol
; 2008 Feb;140(3):279-86
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[Title]
Bone marrow trephine findings in
acute
myeloid leukaemia
with multilineage dysplasia.
Acute
myeloid leukaemia
(
AML
) with multilineage dysplasia (MD) is one of the four main categories
of AML
in the World Health Organization (WHO)
classification
.
The role of bone marrow trephine biopsy (BMTB) histology and immunohistochemistry in the
diagnosis of AML
-MD is currently unclear.
BMTBs were studied in 11 cases
of AML
-MD and two cases of myelodysplasia that subsequently transformed to
AML
.
With respect to conforming to the WHO definition
of AML
, documentation of an increased proportion of immature
myeloid
cells was possible on morphology and counting of immature cells following immunostaining with CD34, CD117 or HLA-DR antibodies.
Based on this relatively small series of cases we show the utility of BMTB and immunohistochemistry as an aid to the
diagnosis of AML
-MD.
This has to be seen
not
just in light of its utility at
diagnosis
, but also the role the diagnostic BMTB would play for purposes of comparison when follow-up BMTBs are submitted in this group of patients.
[MeSH-major]
Bone Marrow Cells / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Myelodysplastic Syndromes / pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antigens, CD34 / analysis. Biomarkers / analysis. Biopsy / methods. Bone Marrow Examination / methods. Cytogenetics.
Disease
Progression. Erythroblasts / pathology. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Megakaryocytes / pathology. Middle Aged.
Myeloid
Cells / pathology. Proto-Oncogene Proteins c-kit / analysis
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(PMID = 17973948.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Biomarkers; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
64.
Huang XF, Luo SK, Xu J, Li J, Xu DR, Wang LH, Yan M, Wang XR, Wan XB, Zheng FM, Zeng YX, Liu Q:
Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia.
Blood
; 2008 Mar 1;111(5):2854-65
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[Title]
Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high
acute
myeloid
leukemia
.
In this study, we found that expression of Aur-A was markedly elevated in bone marrow mononuclear cells (BMMCs) obtained from a significant portion
of de
novo
acute
myeloid
leukemia
(
AML
) patients.
Targeting human primary
AML
cells with Aur-A kinase inhibitory VX-680 led to apoptotic
cell
death in a dose-dependent manner.
Importantly, VX-680-induced
cell
death was preferentially higher in Aur-A-high primary leukemic blasts compared with Aur-A-low
AML
(P < .001) or normal BMMCs (P < .001), suggesting the possible pharmacologic window in targeting Aurora kinase among Aur-A-high VX-680-sensitive
leukemia
patients.
VX-680-induced
cell
death in
AML cell
lines was accompanied by formation of monopolar mitotic spindles, G(2)/M phase arrest, decreased phosphorylated(p)-Akt-1, and increased proteolytic cleavage of procaspase-3 and poly(ADP)ribose polymerase.
Notably, VX-680 increased Bax/Bcl-2 expression ratio, a favorable proapoptotic predictor for drug response and survival in
AML
.
Lastly, VX-680 enhanced the cytotoxic effect of the chemotherapeutic agent etoposide (VP16) on
AML
cells.
Together, we concluded that Aurora kinases were potentially therapeutic targets
for AML
and that Aur-A-high expression may serve as a differential marker for selective treatment.
[MeSH-major]
Apoptosis / drug effects.
Leukemia
,
Myeloid
,
Acute
/ enzymology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Piperazines / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. bcl-2-Associated X Protein / metabolism
[MeSH-minor]
Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Aurora Kinases. Bone Marrow Cells / drug effects. Bone Marrow Cells / enzymology. Bone Marrow Cells / pathology. Caspases / metabolism.
Cell
Division / drug effects.
Cell
Line, Tumor. Child. Drug Screening Assays, Antitumor. Drug Synergism. Enzyme Activation / drug effects. Etoposide / pharmacology. Female. G2 Phase / drug effects. Humans. Male. Middle Aged. Mutation / genetics. fms-Like Tyrosine Kinase 3 / metabolism
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(PMID = 18160664.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Piperazines; 0 / bcl-2-Associated X Protein; 639089-54-6 / VX680; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.22.- / Caspases
65.
Anagnostopoulos C, Jadwat Y, Wood NH, Meyerov R, Lemmer J, Bouckaert M, Feller L:
A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo.
SADJ
; 2007 Oct;62(9):390, 392-3
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[Title]
A report of oral extramedullary
acute
myeloid leukaemia
(
AML
) in an 8-year-old girl with newly diagnosed
AML
-M4Eo.
Acute
myeloid leukaemia
(
AML
), characterized by proliferation of immature neoplastic
myeloid
cells, is uncommon in childhood.
We present a case of an 8-year-old girl with
AML
-M4Eo who had an extramedullary leukaemic tumour in the oral cavity.
[MeSH-major]
Leukemia
, Myelomonocytic,
Acute
/ pathology. Mouth Neoplasms / pathology
[MeSH-minor]
Bone Marrow Neoplasms / pathology. Child.
Diagnosis
, Differential. Eosinophilia / pathology. Fatal Outcome. Female. Humans. Immunophenotyping / methods. Sepsis / drug therapy
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(PMID = 18260548.001).
[ISSN]
1029-4864
[Journal-full-title]
SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging
[ISO-abbreviation]
SADJ
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
South Africa
66.
Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H:
Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis.
Cancer Genomics Proteomics
; 2010 Jul-Aug;7(4):173-80
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[Title]
Use of NG2 (7.1) in
AML
as a tumor marker and its association with a poor prognosis.
We analyzed 70 bone marrow (BM) samples from
acute
myeloid
leukemia
(
AML
) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
We detected NG2(+) cells in
AML
cases with normal karyotype, however,
not
in healthy BM cells.
This means that NG2 qualifies as a reliable
AML
blast tumor marker, enabling monitoring of the course
of AML
independently of, although often associated with, 11q23-aberrations.
While 31% of the patients with NG2(+) cells responded to chemotherapy, 58% of the group with NG2(+) cells did
not
respond (p=0.047).
In conclusion, NG2 detects many, but
not
all 11q23 aberrations and other cases without 11q23 aberrations.
However, it does
not
react with healthy BM cells, thereby contributing to the detection of patients with poor prognosis.
[MeSH-major]
Antigens / analysis. Biomarkers, Tumor / analysis.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Proteoglycans / analysis
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(PMID = 20656983.001).
[ISSN]
1790-6245
[Journal-full-title]
Cancer genomics & proteomics
[ISO-abbreviation]
Cancer Genomics Proteomics
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
67.
McGrath P, Suppiah R, Patton MA:
Re-entering life: paediatric acute myeloid leukaemia at one year post treatment.
Aust J Holist Nurs
; 2005 Oct;12(2):23-34
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[Title]
Re
-entering life: paediatric
acute
myeloid leukaemia
at one year post treatment.
To date, there is scant psychosocial research on the experience of childhood
AML
.
The findings highlight challenges associated with
re
-entering life post-treatment with an emphasis on the ongoing sense of uncertainty, the changed sense of normalcy, and the difficulty of returning to the hospital for check-ups.
A number of recommendations are made including the desirability of providing hospital space for check-ups away from the treatment
area
and the need for ongoing reassurance and support.
[MeSH-major]
Attitude to Health. Holistic Health.
Leukemia
, Myelomonocytic,
Acute
/ psychology. Parent-Child Relations. Parenting / psychology
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(PMID = 19175261.001).
[ISSN]
1322-8803
[Journal-full-title]
The Australian journal of holistic nursing
[ISO-abbreviation]
Aust J Holist Nurs
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
68.
Liu Z, Liu S, Xie Z, Blum W, Perrotti D, Paschka P, Klisovic R, Byrd J, Chan KK, Marcucci G:
Characterization of in vitro and in vivo hypomethylating effects of decitabine in acute myeloid leukemia by a rapid, specific and sensitive LC-MS/MS method.
Nucleic Acids Res
; 2007;35(5):e31
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[Title]
Characterization of in vitro and in vivo hypomethylating effects of decitabine in
acute
myeloid
leukemia
by a rapid, specific and sensitive LC-MS/MS method.
DNA hypermethylation is a common
finding
in malignant cells and has been explored as a therapeutic target for hypomethylating agents (e.g., decitabine).
The assay was validated in
a linear
range from 40 fmol to 200 pmol 5mdC.
This method was initially applied for characterization of decitabine-induced GDM changes in in-vitro-treated
leukemia
cells.
The clinical applicability of this method was then demonstrated in bone marrow samples from patients with
acute
myeloid
leukemia
treated with decitabine.
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[Cites]
Curr Top Microbiol Immunol. 2000;249:135-64
[
10802943.001
]
[Cites]
Rapid Commun Mass Spectrom. 2006;20(7):1117-26
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Mol Biol Evol. 2005 May;22(5):1260-72
[
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[Cites]
J Clin Oncol. 2005 Jun 10;23(17):3897-905
[
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[
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]
[Cites]
Cancer. 2006 Apr 15;106(8):1794-803
[
16532500.001
]
[Cites]
Hum Mol Genet. 2001 Dec 15;10(26):3001-7
[
11751682.001
]
(PMID = 17264127.001).
[ISSN]
1362-4962
[Journal-full-title]
Nucleic acids research
[ISO-abbreviation]
Nucleic Acids Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA102031
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 776B62CQ27 / decitabine; B200GV71QM / 5-methyldeoxycytidine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; G9481N71RO / Deoxyguanosine; M801H13NRU / Azacitidine
[Other-IDs]
NLM/ PMC1865075
69.
Kobayashi T, Nishii K:
[The development of new treatments of acute myelogenous leukemia].
Nihon Rinsho
; 2007 Jan 28;65 Suppl 1:607-10
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[Title]
[The development of new treatments of
acute myelogenous leukemia
].
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy
[MeSH-minor]
Antineoplastic Agents / therapeutic use. Humans.
Leukemia
, Promyelocytic,
Acute
/ drug therapy
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(PMID = 17474468.001).
[ISSN]
0047-1852
[Journal-full-title]
Nihon rinsho. Japanese journal of clinical medicine
[ISO-abbreviation]
Nippon Rinsho
[Language]
jpn
[Publication-type]
Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
19
70.
Tartas NE, Foncuberta MC, Avalos JC:
[Treatment of hematologic neoplasms during pregnancy].
Medicina (B Aires)
; 2007;67(6 Pt 2):729-36
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[Transliterated title]
Tratamiento
de
las neoplasias hematológicas
en
el embarazo.
The most common hematological malignancy in pregnant patients is Hodgkin's lymphoma, but other
diseases
such as chronic and
acute leukemia
or
non
Hodgkin's lymphoma have also been reported.
In the last decade, new drugs have changed the prognostic of
acute
promyelocytic
leukemia
, chronic
myeloid
leukemia
and
non
Hodgkin's lymphoma.
The medical team should offer the most efficient treatment available in order to achieve cure or remission of the
disease
, and also inform on possible risks for the mother and the fetus, as well as those derived from the delay in treatment application.
[MeSH-minor]
Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Benzamides. Enzyme Inhibitors / therapeutic use. Female. Humans. Imatinib Mesylate.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / drug therapy.
Leukemia
, Promyelocytic,
Acute
/ drug therapy. Lymphoma,
Non
-Hodgkin / drug therapy. Piperazines / therapeutic use. Pregnancy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Radiotherapy / adverse effects. Rituximab
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.
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.
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.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
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(PMID = 18422070.001).
[ISSN]
0025-7680
[Journal-full-title]
Medicina
[ISO-abbreviation]
Medicina (B Aires)
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Argentina
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 4F4X42SYQ6 / Rituximab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
[Number-of-references]
71
71.
Bhagwat N, Levine RL:
Metabolic syndromes and malignant transformation: where the twain shall meet.
Sci Transl Med
; 2010 Oct 20;2(54):54ps50
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Recurrent somatic mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes that result in the accumulation
of D
-2-hydroxyglutarate (D-2-HG) have been identified in malignant gliomas and in
acute
myeloid
leukemia
(
AML
).
A report in the current issue of Science describes a germline IDH2 mutation in a subset of patients with a rare metabolic
disorder
--D-2-hydroxyglutaric aciduria-that is similar to mutations seen in cancer patients.
[MeSH-major]
Cell
Transformation, Neoplastic. Glioma / complications. Glutarates / metabolism.
Leukemia
,
Myeloid
,
Acute
/ complications. Metabolism, Inborn Errors / complications
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(PMID = 20962328.001).
[ISSN]
1946-6242
[Journal-full-title]
Science translational medicine
[ISO-abbreviation]
Sci Transl Med
[Language]
eng
[Grant]
United States / Howard Hughes Medical Institute / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Glutarates; 2889-31-8 / alpha-hydroxyglutarate; EC 1.1.1.41 / Isocitrate Dehydrogenase
72.
Hiramatsu A, Miwa H, Shikami M, Ikai T, Tajima E, Yamamoto H, Imai N, Hattori A, Kyo T, Watarai M, Miura K, Satoh A, Itoh M, Imamura A, Mihara H, Katoh Y, Nitta M:
Disease-specific expression of VEGF and its receptors in AML cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17) AML and VEGF/type2 receptor of VEGF in t(8;21) AML.
Leuk Lymphoma
; 2006 Jan;47(1):89-95
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[Title]
Disease
-specific expression of VEGF and its receptors in
AML
cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17)
AML
and VEGF/type2 receptor of VEGF in t(8;21)
AML
.
Various angiogenic factors, such as vascular endothelial growth factor (VEGF) and an associated
molecule
, placenta growth factor (PlGF), are thought to be important for normal and malignant hematopoiesis.
This study examined mRNA expression of VEGF, PlGF and receptors for these
molecules
in
AML
cells and identified the
disease
-specific patterns of expression.
AML
M3 having t(15;17)
abnormality
showed highest expression of VEGF and VEGF receptor type 1 (VEGFR1), suggesting the autocrine pathway of VEGF-VEGFR1.
Then, t(8;21)
AML
demonstrated augmented expression of VEGF and VEGF receptor type 2 (VEGFR2), suggesting VEGF-VEGFR2 autocrine pathway.
Then, addition of VEGFR2 kinase inhibitor in Kasumi-1, a t(8;21)
AML cell
line, resulted in marked inhibition
of cell
growth, although growth inhibitory effect of R2 kinase inhibitor to HL-60 was marginal.
In addition,
cell
cycle analysis study showed S-phase
cell
population reduction by R2 kinase inhibitor in Kasumi-1, but
not
in HL-60.
This observation is thought to be the rationale for novel molecular target therapy directed to angiogenic
molecules
.
[MeSH-major]
Autocrine Communication / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic / genetics. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics
[MeSH-minor]
Adult. Aged.
Cell
Cycle / drug effects.
Cell
Cycle / physiology.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Chromosome Aberrations. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics.
Disease
. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Leukemic / genetics. HL-60 Cells. Humans. Middle Aged. Pregnancy Proteins / biosynthesis. Pregnancy Proteins / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured
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(PMID = 16465716.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Enzyme Inhibitors; 0 / Pregnancy Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 144589-93-5 / placenta growth factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
73.
Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B:
Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
Blood
; 2008 Feb 1;111(3):1575-83
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[Title]
Cytogenetic features of
acute
lymphoblastic
and
myeloid leukemias
in pediatric patients with Down syndrome: an iBFM-SG study.
Children with Down syndrome (DS) have a markedly increased risk of
acute
lymphoblastic
leukemia
(ALL) and
acute
myeloid
leukemia
(
AML
).
To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these
leukemias
, we analyzed 215 DS-ALLs and 189 DS-
AMLs
.
Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-
cell
precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
The HeH DS-ALLs were characterized by gains of the same chromosomes as
non
-DS-HeH, suggesting the same etiology/pathogenesis.
Unlike DS-ALL, the common translocations associated with
non
-DS-
AML
were rare in DS-
AML
, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21.
This series of DS
leukemias
-the largest to date-reveals that DS-ALL is a heterogeneous
disorder
that comprises both t(12;21) and HeH as well as DS-related abnormalities.
Furthermore, this analysis confirms that DS-
AML
is a distinct entity, originating through other genetic pathways than do
non
-DS-
AMLs
, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process.
[MeSH-major]
Down Syndrome / complications. Down Syndrome / genetics.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / complications. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool. Chromosome Aberrations /
classification
. Chromosomes, Human / genetics. Cytogenetics. Female. Genome, Human / genetics. Humans. Infant. Infant, Newborn. Karyotyping. Male
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(PMID = 17971484.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
74.
Chehensse C, Braun T, Morin AS, Stirnemann J, Agranat P, Boukari L, Aras N, Kiladjian JJ, Ziol M, Fenaux P, Fain O:
[Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome].
Rev Med Interne
; 2009 Oct;30(10):886-9
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[Title]
[Extramedullary blastic transformation revealed by a prolonged fever during the course
of a
5q- syndrome].
INTRODUCTION: Fever during a myelodysplastic syndrome can be due to infectious complications, systemic
disease
or
acute
transformation with clonal evolution.
Neither bone marrow nor blood blasts were detected, but
liver
biopsy demonstrated significant blast infiltration compatible with the
diagnosis of
acute
myeloid leukaemia
(
AML
).
CONCLUSION: The absence of blasts in blood or bone marrow does
not
exclude the malignant transformation
of a
myelodysplastic syndrome to
AML
.
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(PMID = 19748163.001).
[ISSN]
0248-8663
[Journal-full-title]
La Revue de medecine interne
[ISO-abbreviation]
Rev Med Interne
[Language]
FRE
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
75.
Unal S, Cakir M, Kuşkonmaz B, Cetin M, Tuncer AM:
Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia.
Turk J Pediatr
; 2009 Jan-Feb;51(1):69-71
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[Title]
Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of
acute
myeloid
leukemia
.
There are few therapeutic options in relapsed or refractory
acute
myeloid
leukemia
patients.
Herein, we present a 15-year-old
acute
myeloid
leukemia
patient who was resistant at relapse and could achieve remission with gemtuzumab ozogamicin at a total dose of 9 mg/
m2
, divided into three doses and delivered to hematopoietic stem-
cell
transplantation; however, the patient relapsed in a short time without application of transplantation.
[MeSH-major]
Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
[MeSH-minor]
Adolescent. Antibodies, Monoclonal, Humanized. Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Hematopoietic Stem
Cell
Transplantation. Humans. Leukocyte Count. Male. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 19378895.001).
[ISSN]
0041-4301
[Journal-full-title]
The Turkish journal of pediatrics
[ISO-abbreviation]
Turk. J. Pediatr.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
76.
Ghafoor T, Zaidi A, Al Nassir I:
Granulocytic sarcoma of the small intestine: an unusual presentation of acute myelogenous leukaemia.
J Pak Med Assoc
; 2010 Feb;60(2):133-5
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[Title]
Granulocytic
sarcoma of the small intestine: an unusual presentation of
acute myelogenous
leukaemia
.
Granulocytic
sarcoma is an extramedullary tumour of primitive
granulocytic
cells.
It can develop at any anatomic site and is often a forerunner to the development of
acute myelogenous
leukaemia
.
Granulocytic
sarcoma of the small intestine presents with abdominal pain and obstruction.
We report a case
of a
17-years-old boy who presented with epigastric pain.
His endoscopy revealed multiple polypoid
lesions
throughout the duodenum and small bowel.
Histopathology and flow cytometery confirmed the
diagnosis of granulocytic
sarcoma associated with
acute myelogenous
leukaemia
.
To our knowledge there have been only two previous case reports of multiple
granulocytic
sarcomas in the small intestine, both of these were adult patients.
This is the first patient in the paediatric age group with multiple
granulocytic
sarcomas of the small intestine.
[MeSH-major]
Intestinal Neoplasms / etiology.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Sarcoma,
Myeloid
/ etiology
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(PMID = 20209703.001).
[ISSN]
0030-9982
[Journal-full-title]
JPMA. The Journal of the Pakistan Medical Association
[ISO-abbreviation]
J Pak Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Pakistan
77.
Brioschi M, Fischer J, Cairoli R, Rossetti S, Pezzetti L, Nichelatti M, Turrini M, Corlazzoli F, Scarpati B, Morra E, Sacchi N, Beghini A:
Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.
Neoplasia
; 2010 Nov;12(11):866-76
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[Title]
Down-regulation of microRNAs 222/221 in
acute myelogenous leukemia
with deranged core-binding factor subunits.
Core-binding factor
leukemia
(CBFL) is a subgroup of
acute
myeloid
leukemia
(
AML
) characterized by genetic mutations involving the subunits of the core-binding factor (CBF).
The leukemogenesis model for CBFL posits that one, or more, gene mutations inducing increased
cell
proliferation and/or inhibition of apoptosis cooperate with CBF mutations for
leukemia
development.
A high expression of KIT is a hallmark
of a
high proportion of CBFL.
Here, we show that MIR-222/221 expression is upregulated after
myeloid
differentiation of normal bone marrow AC133(+) stem progenitor cells.
CBFL blasts with either t(8;21) or inv(16) CBF rearrangements with high expression levels of KIT (CD117) display a significantly lower level of MIR-222/221 expression than
non
-CBFL blasts.
Consistently, we found that the t(8;21) AML1-MTG8 fusion protein binds the MIR-222/221 promoter and induces transcriptional repression
of a
MIR-222/221-LUC reporter.
Because of the highly conserved sequence homology, we demonstrated concomitant MIR-222/221 down-regulation and KIT up-regulation in the 32D/WT1 mouse
cell
model carrying the AML1-MTG16 fusion protein.
This study provides the first hint that CBFL-associated fusion proteins may lead to up-regulation of the KIT receptor by down-regulating MIR-222/221, thus explaining the concomitant occurrence of CBF genetic rearrangements and overexpression of wild type or mutant KIT in
AML
.
[MeSH-major]
Core Binding Factor alpha Subunits / genetics.
Leukemia
,
Myeloid
/ genetics. MicroRNAs / genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Animals. Antigens, CD / genetics. Antigens, CD / metabolism.
Cell
Differentiation / drug effects.
Cell
Differentiation / genetics.
Cell
Line, Tumor. Cells, Cultured. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Down-Regulation. Erythropoietin / pharmacology. Female. Flow Cytometry. Glycoproteins / genetics. Glycoproteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Humans. Male. Middle Aged. Mutation. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Peptides / genetics. Peptides / metabolism. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells
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[ISSN]
1476-5586
[Journal-full-title]
Neoplasia (New York, N.Y.)
[ISO-abbreviation]
Neoplasia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Canada
[Chemical-registry-number]
0 / AC133 antigen; 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor alpha Subunits; 0 / Glycoproteins; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 11096-26-7 / Erythropoietin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
[Other-IDs]
NLM/ PMC2978910
78.
Armand P, Kim HT, DeAngelo DJ, Ho VT, Cutler CS, Stone RM, Ritz J, Alyea EP, Antin JH, Soiffer RJ:
Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation.
Biol Blood Marrow Transplant
; 2007 Jun;13(6):655-64
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[Title]
Impact of cytogenetics on outcome
of de
novo and therapy-related
AML
and MDS after allogeneic transplantation.
Cytogenetics has an important impact on the prognosis of patients undergoing allogeneic hematopoietic stem
cell
transplantation (HSCT) for
acute myelogenous leukemia
(
AML
) or myelodysplastic syndromes (MDS).
Also, the impact of cytogenetics in the growing population of patients with therapy-related
disease
has
not
been completely elucidated.
In this study, we retrospectively analyzed data on 556 patients with
AML
or MDS transplanted at our institution.
We examined, in multivariate analyses, the contribution of cytogenetics to survival, relapse, and nonrelapse mortality for the 476 patients with
de
novo
disease
.
We then applied this grouping scheme to the 80 patients with therapy-related
disease
.
Our proposed 3-group cytogenetic
classification
outperformed the established grouping schemes for both
de
novo and therapy-related
disease
.
When classified by this new scheme, cytogenetics was the strongest prognostic factor for overall survival in our cohort, through its impact on the risk of relapse (and
not
on nonrelapse mortality).
After accounting for cytogenetics, patients with therapy-related
AML
or MDS had an equivalent outcome to those with
de
novo
disease
.
This study demonstrates the impact of cytogenetics on the risk of relapse and death for patients with both
de
novo and therapy-related
disease
undergoing transplantation; it also emphasizes the necessity of using cytogenetics to stratify patients entering clinical trials, and provides a system for doing so, which can be validated in a multi-institutional database.
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(PMID = 17531775.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / U19 AI 29530; United States / NHLBI NIH HHS / HL / P01 HL070149; United States / NCI NIH HHS / CA / T32 CA009172; United States / NIAID NIH HHS / AI / AI029530-14; United States / NHLBI NIH HHS / HL / P01 HL 070149; United States / NIAID NIH HHS / AI / U19 AI029530
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS25237; NLM/ PMC2743535
79.
Carpiuc KT, Stephens JM, Botteman MF, Feng W, Hay JW:
A review of the clinical and economic outcomes of imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia.
Expert Opin Pharmacother
; 2007 Nov;8(16):2775-87
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[Title]
A review of the clinical and economic outcomes of imatinib in Philadelphia chromosome-positive
acute
lymphoblastic
leukemia
.
Philadelphia chromosome-positive (Ph+)
acute
lymphoblastic
leukemia
(ALL) is a rare, high-risk, aggressive form of
acute leukemia
, affecting primarily adults and the elderly.
Patients with high-risk forms of ALL typically have extremely poor prognosis and incur high
disease
-related costs.
Successful use of imatinib in patients with Ph+ chronic
myelogenous leukemia
(CML) has led to the administration of imatinib in recent clinical studies for patients with Ph+ALL.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Piperazines / therapeutic use. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
[MeSH-minor]
Benzamides. Costs and Cost Analysis. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Quality of Life. Stem
Cell
Transplantation
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.
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(PMID = 17956198.001).
[ISSN]
1744-7666
[Journal-full-title]
Expert opinion on pharmacotherapy
[ISO-abbreviation]
Expert Opin Pharmacother
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
[Number-of-references]
70
80.
Walter K, Cockerill PN, Barlow R, Clarke D, Hoogenkamp M, Follows GA, Richards SJ, Cullen MJ, Bonifer C, Tagoh H:
Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.
Oncogene
; 2010 May 20;29(20):2927-37
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[Title]
Aberrant expression of CD19 in
AML
with t(8;21) involves a poised chromatin structure and PAX5.
Co-expression of lymphoid and
myeloid molecules
is a well-known feature of
acute
myeloblastic
leukemia
(
AML
) with t(8;21).
These cells consistently express the B-
cell
-specific transcription factor PAX5, and the B-
cell
-specific
cell
surface protein CD19.
We show that CD19 chromatin exists in a poised configuration in
myeloid
progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation.
Our results also show a positive correlation between PAX5 and CD19 expression in t(8;21)-positive
AML
cells and demonstrate that PAX5 binds to the promoter and enhancer of CD19 gene and remodels chromatin structure at the promoter.
This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role
of a
progenitor-specific chromatin configuration in
myeloid
leukemia
.
[MeSH-major]
Antigens, CD19 / genetics. B-
Cell
-Specific Activator Protein / genetics. Chromatin / chemistry. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic / genetics
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(PMID = 20208555.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Chromatin; 0 / PAX5 protein, human
81.
Scholl S, Theuer C, Scheble V, Kunert C, Heller A, Mügge LO, Fricke HJ, Höffken K, Wedding U:
Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia.
Eur J Haematol
; 2008 Mar;80(3):208-15
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[Title]
Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with
acute
myeloid leukaemia
.
BACKGROUND: Nucleophosmin (NPM1) and Flt3 internal tandem duplications (Flt3-ITD mutations) represent the most frequent molecular aberrations in patients with
acute
myeloid
leukemia
(
AML
).
While NPM1 mutations are associated with favourable prognosis in younger
AML
patients, Flt3-ITD mutations reflect an unfavourable prognostic factor in these patients.
So far, especially NPM1 mutations have
not
yet been evaluated exclusively in older patients.
PATIENTS AND METHODS: We retrospectively analysed the prevalence of NPM1 and Flt3-ITD mutations and its association with complete remission (CR), and survival in 99 elderly patients (median age 71 yr, range 60-85 yr) newly diagnosed
for AML
.
Interestingly, there is no significant difference in overall survival between group 1 and group 2 (
Log
-rank test P = 0.22, median 440 d vs. 1125 d).
In contrast, patients carrying a Flt3-ITD mutation had a significant worse overall survival compared to wildtype patients (P = 0.03, median 210
d for
group 3 + 4 vs. 634
d for
group 1 + 2) while no difference of CR rate could be observed (42.8% vs. 48.9%, P = 0.91).
CONCLUSION: As elderly but medically fit patients with
AML
carrying a NPM1 mutation have a high CR rate, age itself should
not
be a barrier for induction treatment.
However, new therapeutic concepts of postremission therapy (e.g. allogeneic stem
cell
transplantation after dose-reduced conditioning) should be considered for these patients in first CR.
[MeSH-major]
Gene Duplication.
Leukemia
,
Myeloid
,
Acute
/ genetics. Nuclear Proteins / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Aged. Aged, 80 and over. Cohort Studies.
Disease
-Free Survival. Female. Gene Frequency. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies
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(PMID = 18081718.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
82.
Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E:
Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
Pediatr Blood Cancer
; 2006 Feb;46(2):266
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[Title]
Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with
acute
non
-
lymphoblastic
leukemia
.
[MeSH-major]
Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ complications
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.
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.
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.
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(PMID = 16078222.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin
83.
Tan L, Xu B, Liu R, Liu H, Tan H, Huang W:
Gene therapy for acute myeloid leukemia using Sindbis vectors expressing a fusogenic membrane glycoprotein.
Cancer Biol Ther
; 2010 Mar 1;9(5):350-7
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[Title]
Gene therapy for
acute
myeloid
leukemia
using Sindbis vectors expressing a fusogenic
membrane
glycoprotein.
AML
has a dismal prognosis.
It was previously shown that the expression of gene coding for the hyperfusogenic gibbon ape
leukemia
virus envelope glycoprotein (GALV.fus) can efficiently kill leukemic cells.
However, target killing effect of GALV.fus on
leukemia
cells may be limited.
Viral vectors, such as retroviruses and adenoviruses, have been developed to deliver heterologous genes into tumors in vivo, but these vectors have some limitations for gene therapy of
leukemia
.
We found that Laminin-R was obviously expressed in HL-60 and primary human
AML
cells, but weakly expressed in K562 cells and blood samples of normal human.
So we reasoned that Sindbis-virus-based vectors might be ideal for target gene transfer of GALV.fus to
acute
myeloid
leukemic
cell
.
It was shown that Sindbis virus efficiently transduced human
acute
myeloid
leukemic cells with high expression of Laminin-R and exhibited potent cytopathic potential.
What is more, we found that CFU-GMs were significantly reduced after Sindbis virus carrying GALV.fus transduced human primary
AML
cells.
Sindbis virus carrying GALV.fus was active against human
AML
xenografts in vivo.
Taken together, we concluded that Sindbis virus carrying GALV.fus may be an useful strategy for gene therapy of
acute
myeloid
leukemia
.
[MeSH-minor]
Adenoviridae / genetics. Granulocyte-Macrophage Progenitor Cells. Humans.
Leukemia
Virus, Gibbon Ape / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy.
Membrane
Glycoproteins / genetics
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[CommentIn]
Cancer Biol Ther. 2010 Mar 1;9(5):358-61
[
20104027.001
]
(PMID = 20061812.001).
[ISSN]
1555-8576
[Journal-full-title]
Cancer biology & therapy
[ISO-abbreviation]
Cancer Biol. Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Membrane Glycoproteins
84.
Rheingold SR:
Acute myeloid leukemia in a child with hereditary thrombocytopenia.
Pediatr Blood Cancer
; 2007 Jan;48(1):105-7
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[Title]
Acute
myeloid
leukemia
in a child with hereditary thrombocytopenia.
A child with a known
diagnosis of
an autosomal dominant macrothrombocytopenia, Fechtner Syndrome, developed
acute
myeloid
leukemia
(
AML
).
Recently the
disease
gene for the inherited macrothrombocytopenias has been identified as MYH9, encoding
for non
-muscle myosin heavy chain-A.
MYH9 has never been associated with the development of
acute leukemia
, but MYH11 is disrupted in the M4 eosinophilia sub-type
of AML
(inv16).
The patients leukemic blasts did carry the common t(8;21) which yields an AML1-ETO fusion protein that inhibits
AML
-1.
[MeSH-major]
Blood Coagulation Disorders, Inherited / genetics. Chromosome Disorders / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Thrombocytopenia / genetics
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16276527.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
85.
Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T:
Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
Cancer Genet Cytogenet
; 2009 Oct;194(1):38-43
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[Title]
Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in
acute
myeloid
leukemia
with multilineage dysplasia.
Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in
acute
lymphoblastic
leukemia
.
We describe here a novel case of
acute
myeloid
leukemia
(
AML
) with double idic(21)(p11.2).
A 35-year-old man was diagnosed as having
de
novo
AML
with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
These results suggest that the idic(21)(p11.2) could be implicated also in the pathogenesis
of AML
through amplification of genes including RUNX1 located on 21q.
[MeSH-major]
Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease
. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping
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(PMID = 19737652.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
86.
Abdel Alim A, Youssef SR, Farouk HM:
The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with acute myeloid leukemia.
Egypt J Immunol
; 2010;17(1):9-18
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[Title]
The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with
acute
myeloid
leukemia
.
Aberrations in the
cell
cycle control are often observed in tumors and might even be mandatory in tumor development.
There are few molecular biologic determinants that may be prognostic for patients with
acute
myeloid
leukemia
(
AML
).
To investigate the importance
of cell
cycle defects in
AML
, the cellular levels of cyclin E and the cyclin-dependent kinase inhibitor P27 (Kip 1) were evaluated in thirty
AML
patients (11 males and 19 females) diagnosed by standard clinical, morphological and immunophenotypic criteria and staged according to the FAB
classification
.
Using immunoblot analysis, cyclin E and P27 were detected in blast cells
of AML
patients who were then treated by the standard
AML
chemotherapeutic protocol and were followed up.
With respect to cyclin E, it was detected in 9/30(30%)
AML
cases among them 13.3% (4/30 cases) exhibited very strong bands while 16.6% (5/30 cases) showed faint bands.
Cyclin E was high among M4/M5 cases and low among M3 cases and showed a statistically significant positive correlation with percentage of blast cells, aberrant phenotype and abnormal karyotype at
diagnosis
.
All our
AML
cases exhibited P27 at low and high levels as seen in 19/30 (63.4%) and 11/30 (36.6%) cases, respectively.
P27 showed a statistically significant negative correlation to the percentage of blasts at
diagnosis
and a significant positive correlation with achievement of CR.
The present study suggested that levels
of cell
cycle regulators cyclin E and P27 can be used as a useful prognostic molecular markers in
AML
patients.
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(PMID = 22053605.001).
[ISSN]
1110-4902
[Journal-full-title]
The Egyptian journal of immunology
[ISO-abbreviation]
Egypt J Immunol
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cyclin E; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
87.
Rytting M, Ravandi F, Estey E, Cortes J, Faderl S, Garcia-Manero G, Jeha S, Ouzounian S, Pierce S, Kantarjian H:
Intensively timed combination chemotherapy for the induction of adult patients with acute myeloid leukemia: long-term follow-up of a phase 2 study.
Cancer
; 2010 Nov 15;116(22):5272-8
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[Title]
Intensively timed combination chemotherapy for the induction of adult patients with
acute
myeloid
leukemia
: long-term follow-up
of a
phase 2 study.
BACKGROUND: Despite advances in therapy, the majority of adult patients diagnosed with
acute
myeloid
leukemia
(
AML
) develop
disease
recurrence and die of their
disease
.
Early intensification of treatment
for AML
using timed sequential therapy (TST) has been proposed as a means of improving the survival outcome in children.
The Children's Cancer Group demonstrated that children with
AML
who were randomized to receive 2 courses of daunorubicin, cytarabine, thioguanine, etoposide, and dexamethasone (the DCTER regimen) given 10 days apart had an improved event-free survival (EFS) and
disease
-free survival (DFS) (42% ± 7% and 55% ± 9%, respectively, at 2 years).
Reports have suggested an improved outcome in adult patients with
AML
using TST (at the cost of increased toxicity).
The current study was conducted to evaluate the feasibility and effectiveness of the intensively timed DCTER regimen
for non
-core-binding factor
AML
in adult patients aged <50 years.
The timed sequential DCTER regimen had a lower complete remission (CR) rate when compared with the IA combination,, (71% vs 80%, respectively), but this appeared to be counterbalanced by a higher long-term
leukemia
-free survival rate using the intensified regimen (48% vs 30%, respectively) in patients who achieved a CR (P = .06).
CONCLUSIONS: The intensively timed regimen of DCTER was found to induce durable remissions in adult patients with
AML
, including those patients with high-risk
disease
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
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.
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CYTARABINE
.
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THIOGUANINE
.
Hazardous Substances Data Bank.
DAUNORUBICIN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
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[Copyright]
Copyright © 2010 American Cancer Society.
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(PMID = 20665501.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DCTER protocol
88.
Bullinger L, Krönke J, Schön C, Radtke I, Urlbauer K, Botzenhardt U, Gaidzik V, Carió A, Senger C, Schlenk RF, Downing JR, Holzmann K, Döhner K, Döhner H:
Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis.
Leukemia
; 2010 Feb;24(2):438-49
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[Title]
Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal
acute
myeloid
leukemia
using high-resolution single-nucleotide polymorphism analysis.
As
acute
myeloid
leukemia
(
AML
) represents a genetically heterogeneous
disease
, this technology might prove helpful, especially for cytogenetically normal
AML
(CN-
AML
) cases.
Thus, we performed high-resolution SNP analyses in 157 adult cases of CN-
AML
.
Furthermore, we identified two cases with a cryptic t(6;11) as well as several
non
-recurrent aberrations pointing to
leukemia
-relevant regions.
These data show the potential of high-resolution SNP analysis for identifying genomic regions of potential pathogenic and clinical relevance in
AML
.
[MeSH-major]
Gene Dosage.
Leukemia
,
Myeloid
,
Acute
/ genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy / genetics
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(PMID = 20016533.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
89.
Fischbach NA, Rozenfeld S, Shen W, Fong S, Chrobak D, Ginzinger D, Kogan SC, Radhakrishnan A, Le Beau MM, Largman C, Lawrence HJ:
HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo.
Blood
; 2005 Feb 15;105(4):1456-66
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[Title]
HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem
cell
expansion and
acute
myeloid
leukemia
in vivo.
Dysregulated HOX gene expression profoundly effects the proliferation and differentiation of hematopoietic stem cells (HSCs) and committed progenitors, and aberrant activation of HOX genes is a common event in human
myeloid
leukemia
.
HOXB6 is frequently overexpressed in human
acute
myeloid
leukemia
(
AML
).
We also explored structure-function relationships using mutant HOXB6 proteins unable to bind to DNA or a key HOX-binding partner, pre-B-
cell
leukemia
transcription factor-1 (PBX1).
Additionally, we investigated the potential cooperative interaction with
myeloid
ecotropic viral integration site 1 homolog (MEIS1).
In vivo, HOXB6 expanded HSCs and
myeloid
precursors while inhibiting erythropoiesis and lymphopoiesis.
Overexpression of HOXB6 resulted in
AML
with a median latency of 223 days.
Coexpression of MEIS1 dramatically shortened the onset
of AML
.
Cytogenetic analysis
of a
subset of HOXB6-induced
AMLs
revealed recurrent deletions of chromosome bands 2D-E4, a region frequently deleted in HOXA9-induced
AMLs
.
In vitro, HOXB6 immortalized a factor-dependent myelomonocytic precursor capable
of granulocytic
and monocytic differentiation.
[MeSH-major]
Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology.
Cell
Transformation, Neoplastic / pathology. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics.
Leukemia
,
Myeloid
/ blood.
Myeloid
Progenitor Cells / metabolism.
Myeloid
Progenitor Cells / pathology
[MeSH-minor]
Acute
Disease
. Animals.
Cell
Differentiation / genetics.
Cell
Line, Transformed.
Cell
Proliferation. Erythropoiesis / genetics. Female. Karyotyping. Lymphopoiesis / genetics. Mice. Mice, Congenic. Mice, Inbred C57BL. Neoplasm Proteins / physiology. Phenotype. Time Factors
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PMID 15522959 (Special Collections)
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(PMID = 15522959.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / DK48642
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Hoxb6 protein, mouse; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein
90.
Kaufman DW, Anderson TE, Issaragrisil S:
Risk factors for leukemia in Thailand.
Ann Hematol
; 2009 Nov;88(11):1079-88
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[Title]
Risk factors for
leukemia
in Thailand.
A case-control study of adult-onset
leukemia
was conducted in Bangkok, Thailand to explore the contribution of cellular telephone use and other factors to the etiology of the
disease
; 180 cases (87
acute
myeloblastic
leukemia
, 40
acute
lymphoblastic
leukemia
, 44 chronic
myelogenous leukemia
, eight chronic
lymphocytic
leukemia
, one unclassified
acute leukemia
) were compared with 756 age- and sex-matched hospital controls.
Myeloid
leukemia
(
acute
and chronic combined) was associated with benzene (OR, 3.9; 95% confidence interval, 1.3-11), a nonspecific group of other solvents (2.3; 1.1-4.9), occupational pesticides that were mostly unspecified (3.8; 2.1-7.1), and working with or near powerlines (4.3; 1.3-15).
[MeSH-major]
Leukemia
/ epidemiology
[MeSH-minor]
Adult. Aged. Benzene / adverse effects. Case-Control Studies.
Cell
Phones. Electromagnetic Fields / adverse effects. Female. Humans.
Leukemia
, Radiation-Induced / epidemiology.
Leukemia
, Radiation-Induced / etiology. Male. Middle Aged. Occupational Exposure. Pesticides / adverse effects. Radiography / adverse effects. Risk Factors. Smoking / epidemiology. Solvents / adverse effects. Thailand / epidemiology. Young Adult
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.
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(PMID = 19294385.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Pesticides; 0 / Solvents; J64922108F / Benzene
91.
Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S:
Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
Haematologica
; 2005 Jun;90(6):776-84
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[Title]
Fludarabine and cytarabine as continuous sequential infusion for elderly patients with
acute
myeloid
leukemia
.
BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects
of a
therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with
acute
myeloid
leukemia
(
AML
).
DESIGN AND METHODS: Sixty-three patients with
non
-M3
AML
, median age 69 years (range 61-81), were accrued.
Twenty-four patients (38%) had
AML
secondary to myelodysplastic syndrome.
Patients achieving complete remission (CR) were intended to receive an additional course, followed by autologous stem
cell
transplantation (ASCT).
The median overall and
disease
-free survival were both 10 months.
Results in terms of CR achievement, CD34+
cell
collection and ASCT feasibility.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Vidarabine / analogs & derivatives
[MeSH-minor]
Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis.
Disease
-Free Survival. Female. Humans. Male. Middle Aged. Myelodysplastic Syndromes / complications. Stem
Cell
Transplantation. Treatment Outcome
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CYTARABINE
.
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FLUDARABINE
.
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VIDARABINE
.
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(PMID = 15951290.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
92.
Balaian L, Ball ED:
Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukemia correlates with the expression of protein kinase Syk.
Leukemia
; 2006 Dec;20(12):2093-101
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[Title]
Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in
acute
myeloid
leukemia
correlates with the expression of protein kinase Syk.
Acute
myeloid
leukemia
(
AML
) cells express the
cell
surface antigen CD33 that, upon ligation with a monoclonal antibody (mAb), is a downregulator
of cell
growth in a Syk-dependent manner.
An anti-CD33 mAb coupled to a toxin, gemtuzumab ozogamicin (GO), is used for the treatment
of AML
(Mylotarg).
Therefore, we investigated whether the response
of AML
cells to GO treatment also depends on Syk expression.
Forty primary
AML
samples (25 Syk-positive and 15 Syk-negative) were tested for their response to the anti-proliferative effects of GO and unmodified anti-CD33 mAb.
A correlation between Syk expression and the response of
leukemia
cells to GO and anti-CD33 mAb was found.
'Blocking' of Syk by small interfering RNA resulted in unresponsiveness
of AML
cells to both GO and anti-CD33 mAb-mediated cytotoxicity.
Syk upregulation by the
de
-methylating agent 5-azacytidine (5-aza) induced
re
-expression of Syk in some cases, resulting in enhanced GO and anti-CD33-mediated inhibition of
leukemia
cell
growth.
Thus, the cytotoxicity of both GO and anti-CD33 in primary
AML
samples was associated with Syk expression.
5-Aza restored Syk and increased the sensitivity of originally Syk-negative,
non
-responsive cells to CD33 ligation to levels of Syk-positive cells.
[MeSH-major]
Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotoxins / pharmacology. Intracellular Signaling Peptides and Proteins / analysis.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Protein-Tyrosine Kinases / analysis
[MeSH-minor]
Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Azacitidine / pharmacology.
Cell
Line, Tumor. Humans. RNA, Small Interfering. Sialic Acid Binding Ig-like Lectin 3
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.
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(PMID = 17051243.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; M801H13NRU / Azacitidine
93.
Scholl S, Krause C, Loncarevic IF, Müller R, Kunert C, Wedding U, Sayer HG, Clement JH, Höffken K:
Specific detection of Flt3 point mutations by highly sensitive real-time polymerase chain reaction in acute myeloid leukemia.
J Lab Clin Med
; 2005 Jun;145(6):295-304
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[Title]
Specific detection of Flt3 point mutations by highly sensitive real-time polymerase chain reaction in
acute
myeloid
leukemia
.
Among activating class III receptor tyrosine kinase (Flt3) mutations, internal tandem duplications of Flt3 (Flt3-ITD) are detected in about 25% of patients with
acute
myeloid
leukemia
(
AML
).
Based on individual Flt3-TKD mutations, we designed patient-specific primers to perform a highly sensitive polymerase chain reaction (PCR) assay for rapid detection of minimal residual
disease
(MRD).
[MeSH-major]
Leukemia
,
Myeloid
/
diagnosis
.
Leukemia
,
Myeloid
/ genetics. Point Mutation. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
[MeSH-minor]
Acute
Disease
. Base Sequence. DNA Primers. Genetic Testing / methods. Humans. Molecular Sequence Data. Retrospective Studies. Sensitivity and Specificity. fms-Like Tyrosine Kinase 3
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(PMID = 15976757.001).
[ISSN]
0022-2143
[Journal-full-title]
The Journal of laboratory and clinical medicine
[ISO-abbreviation]
J. Lab. Clin. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
94.
Tang X, Long C, Wang C, Xiao G:
[Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
; 2009 Sep;34(9):886-91
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[Title]
[Expression of DLK1 gene in
acute
leukemias
and its function in erythroid differentiation of K562
cell
line].
OBJECTIVE: To determine the expression of DLK1 gene in
acute
leukemias
(AL) and its function in erythroid differentiation of K562 cells.
METHODS: We detected the expression of DLK1 gene in 65 different
acute leukemia
categories (a test group) and 34 normal bone marrow controls (a control group) with RT-PCR.
The K562
cell
line was induced to erythroid differentiation by hemin.
RESULTS: Both
leukemia
cells and normal marrow cells expressed DLK1.
The expression of DLK1 mRNA in patients in the test group was higher than that in the control group (P=0.018), while there was no significance between
acute
lymphoblastic
leukemia
and
acute myelogenous leukemia
(P>0.05).The expression of DLK1 mRNA in the test group at onset had no relation with the WBC and platelet count in the total peripheral blood, and the same was true for blast
cell
rates in bone marrow cells.The level of DLK1 protein in the test group was higher than that in the control group, which was consistent with the mRNA expression (P=0.042).
CONCLUSION: DLK1 gene may be involved in
leukemia
,but the mRNA level of DLK1 has no relation with some clinical characteristics of AL patients at onset.
[MeSH-major]
Cell
Differentiation / genetics.
Cell
Transformation, Neoplastic / genetics. Erythroid Cells / pathology. Intercellular Signaling Peptides and Proteins / metabolism.
Leukemia
/ genetics.
Membrane
Proteins / metabolism
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Case-Control Studies. Child. Child, Preschool. Erythroid Precursor Cells / pathology. Female. Humans. K562 Cells. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult
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(PMID = 19779261.001).
[ISSN]
1672-7347
[Journal-full-title]
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
[ISO-abbreviation]
Zhong Nan Da Xue Xue Bao Yi Xue Ban
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RNA, Messenger
95.
Harkey MA, Kaul R, Jacobs MA, Kurre P, Bovee D, Levy R, Blau CA:
Multiarm high-throughput integration site detection: limitations of LAM-PCR technology and optimization for clonal analysis.
Stem Cells Dev
; 2007 Jun;16(3):381-92
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[Title]
Multiarm high-throughput integration site detection: limitations
of LAM
-PCR technology and optimization for clonal analysis.
Retroviral integration provides a unique and heritable genomic tag
for a
target
cell
and its progeny, enabling studies of clonal composition and repopulation kinetics after gene transfer into hematopoietic stem cells.
The clonal tracking method,
linear
amplification-mediated polymerase chain reaction (
LAM
-PCR) is widely employed to follow the hematopoietic output of retrovirally marked stem cells.
Here we examine the capabilities and limitations of conventional
LAM
-PCR to track individual clones in a complex multiclonal mix.
Using artificial mixtures of retrovirally marked, single-
cell
-derived clones, we demonstrate that
LAM
-PCR fails to detect 30-40% of the clones, even after exhaustive analysis.
Furthermore, the relative abundance of specific clones within a mix is
not
accurately represented, deviating by as much as 60-fold from their true abundance.
We describe an optimized, multiarm, high-throughput modification
of LAM
-PCR that improves the global detection capacity to greater than 90% with exhaustive sampling, facilitates accurate estimates of the total pool size from smaller samplings, and provides a rapid, cost-effective approach to the generation of large insertion-site data bases required for evaluation of vector integration preferences.
Thus, although
LAM
-PCR is a powerful tool for identification of integration sites and for estimations of clonal complexity, it fails to provide the semiquantitative information necessary for direct, reliable tracking of individual clones in a chimeric background.
[MeSH-major]
Cell
Separation / methods. Clone Cells / physiology. Polymerase Chain Reaction / methods
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(PMID = 17610368.001).
[ISSN]
1547-3287
[Journal-full-title]
Stem cells and development
[ISO-abbreviation]
Stem Cells Dev.
[Language]
eng
[Grant]
United States / NHGRI NIH HHS / HG / 5U54 HG00243; United States / NIDDK NIH HHS / DK / DK56456-02; United States / NHLBI NIH HHS / HL / HL077231; United States / NHLBI NIH HHS / HL / P01 HL53750-09; United States / NIDDK NIH HHS / DK / R01 DK52997-05; United States / NIDDK NIH HHS / DK / R01 DK61844-01
[Publication-type]
Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
147336-22-9 / Green Fluorescent Proteins
96.
Li H, Guo L, Jie S, Liu W, Zhu J, Du W, Fan L, Wang X, Fu B, Huang S:
Berberine inhibits SDF-1-induced AML cells and leukemic stem cells migration via regulation of SDF-1 level in bone marrow stromal cells.
Biomed Pharmacother
; 2008 Nov;62(9):573-8
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[Title]
Berberine inhibits SDF-1-induced
AML
cells and leukemic stem cells migration via regulation of SDF-1 level in bone marrow stromal cells.
Berberine plays a prominent role on the control of tumor
cell
invasion and migration.
In this study, we investigated the effects of berberine on the SDF-1-induced HL-60 cells, primary
acute
myeloid
leukemia
(
AML
) cells and leukemic stem cells (LSCs) migration.
Transwell migration chambers (8 microm) were used to assess the role of berberine on leukemic
cell
migration; Flow cytometry was used to analyze the role of berberine on the CXCR4 expression; SDF-1 protein level secreted by bone marrow stromal cells (BMSCs) was evaluated by ELISA.
Results demonstrated that berberine could partly inhibit SDF-1-induced
AML
cells as well as LSCs migration.
Berberine could reduce SDF-1 protein level secreted by BMSCs in the microenvironment but
not
affect CXCR4 expression on HL-60
cell membrane
, and we hypothesized that berberine could inhibit
AML
cells migration partly by reducing the secreting of SDF-1 by BMSCs and inhibiting HERG1 K(+) channels of leukemic cells.
Therefore, it is speculated that berberine might be a potentially effective agent for prevention of
leukemia
.
[MeSH-major]
Anticarcinogenic Agents / pharmacology. Berberine / pharmacology. Bone Marrow Cells / drug effects. Chemokine CXCL12 / metabolism.
Leukemia
,
Myeloid
,
Acute
/ pathology. Neoplastic Stem Cells / drug effects
[MeSH-minor]
Adolescent. Adult. Aged.
Cell
Movement. Child. Depression, Chemical. Female. HL-60 Cells. Humans. Male. Middle Aged
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(PMID = 18805669.001).
[ISSN]
1950-6007
[Journal-full-title]
Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
[ISO-abbreviation]
Biomed. Pharmacother.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
France
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Chemokine CXCL12; 0I8Y3P32UF / Berberine
97.
Cooper T, Ayres M, Nowak B, Gandhi V:
Biochemical modulation of cytarabine triphosphate by clofarabine.
Cancer Chemother Pharmacol
; 2005 Apr;55(4):361-8
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PURPOSE: Clofarabine has proven to be effective in the treatment of adult and pediatric
acute myelogenous leukemia
(
AML
).
To investigate if clofarabine could be used with success in biochemical modulation strategies, we investigated the biochemical modulation of cytarabine triphosphate (ara-CTP) by clofarabine in
a myeloid
leukemia
cell
line and the effect of this combination on cytotoxicity.
This level was achieved at the maximum tolerated dose for adult and pediatric patients with
AML
.
Preincubation with ara-C did
not
affect the triphosphate form, but it lowered clofarabine monophosphate.
Clonogenic assays revealed that the combination of clofarabine and ara-C produced synergistic killing
of myeloid
leukemia
cells.
CONCLUSIONS: These findings demonstrate that combination of clofarabine followed by ara-C results in a biochemical modulation of ara-CTP and synergistic
cell
kill.
These studies provide a compelling rationale for clinical trials using this combination regimen for adult and pediatric patients with
AML
.
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(PMID = 15723262.001).
[ISSN]
0344-5704
[Journal-full-title]
Cancer chemotherapy and pharmacology
[ISO-abbreviation]
Cancer Chemother. Pharmacol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / CA57629
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
Germany
[Chemical-registry-number]
0 / Adenine Nucleotides; 0 / Arabinonucleosides; 04079A1RDZ / Cytarabine; 762RDY0Y2H / clofarabine; EC 1.17.4.- / Ribonucleotide Reductases
98.
Karst C, Heller A, Claussen U, Gebhart E, Liehr T:
Detection of cryptic chromosomal aberrations in the in vitro non-proliferating cells of acute myeloid leukemia.
Int J Oncol
; 2005 Aug;27(2):355-9
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[Title]
Detection of cryptic chromosomal aberrations in the in vitro
non
-proliferating cells of
acute
myeloid
leukemia
.
A total of 22
acute
myeloid
leukemia
(
AML
) cases were analyzed by
cell
-specific comparative genomic hybridization (micro-CGH).
These results lead to two conclusions: i) in the in vitro
non
-proliferating population
of AML
tumor cells one can detect cryptic chromosomal aberrations, which might constitute tumor markers of diagnostic and prognostic value;.
[MeSH-major]
Bone Marrow / metabolism. Chromosome Aberrations.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Aged, 80 and over.
Cell
Proliferation. Chromosome Banding. Female. Genome, Human. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Male. Nucleic Acid Hybridization / methods. Pilot Projects
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(PMID = 16010415.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
99.
Lozzi GP, Massone C, Citarella L, Kerl H, Cerroni L:
Rimming of adipocytes by neoplastic lymphocytes: a histopathologic feature not restricted to subcutaneous T-cell lymphoma.
Am J Dermatopathol
; 2006 Feb;28(1):9-12
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[Title]
Rimming of adipocytes by neoplastic lymphocytes: a histopathologic feature
not
restricted to subcutaneous T-
cell
lymphoma.
Subcutaneous panniculitis-like T-
cell
lymphoma (SPTCL) is a rare cytotoxic T-
cell
lymphoma of the skin presenting with histopathologic features simulating those
of a
lobular panniculitis.
The presence of neoplastic T-lymphocytes forming a rim around the individual fat cells in the subcutaneous lobules, so-called "rimming" of adipocytes, is considered a characteristic
morphologic
feature of this type of cutaneous lymphoma.
In this study we reviewed a series of 45 biopsy specimens of primary and secondary cutaneous B- and T-
cell
lymphomas and one
of myeloid
leukemia
involving the subcutaneous tissues and showing rimming of adipocytes (subcutaneous panniculitis-like T-
cell
lymphoma: n = 16; mycosis fungoides, tumor stage: n = 3; aggressive epidermotropic CD8(+) T-
cell
lymphoma: n = 2; cutaneous gamma/delta T-
cell
lymphoma: n = 4; extranodal NK/T-
cell
lymphoma, nasal type: n = 4; cutaneous medium-large pleomorphic T-
cell
lymphoma,
NOS
: n = 5; CD4(+)/CD56(+) hematodermic neoplasm (blastic NK-
cell
lymphoma): n = 7; secondary cutaneous large B-
cell
lymphoma: n = 3; secondary cutaneous lymphoplasmacytic lymphoma: n = 1; specific cutaneous manifestations of
acute myelogenous leukemia
: n = 1).
We could demonstrate that rimming of adipocytes by neoplastic cells can be recognized
not
only in subcutaneous panniculitis-like T-
cell
lymphoma, but also in several different entities of malignant lymphoma with skin involvement.
Precise
classification of
cases with prominent involvement of the subcutaneous tissues can only be achieved upon precise correlation of clinicopathologic and phenotypic features.
Rimming of adipocytes should
not
be considered specific of subcutaneous panniculitis-like T-
cell
lymphoma.
[MeSH-major]
Adipocytes / pathology. Lymphoma, B-
Cell
/ pathology. Lymphoma, T-
Cell
/ pathology. Skin Neoplasms / pathology. T-Lymphocytes / pathology
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Gene Rearrangement. Genes, T-
Cell
Receptor gamma / genetics. Humans. Immunoglobulin Heavy Chains / genetics. Male. Middle Aged. Panniculitis / metabolism. Panniculitis / pathology. Receptors, Antigen, T-
Cell
, gamma-delta / genetics. Receptors, Antigen, T-
Cell
, gamma-delta / metabolism
MedlinePlus Health Information.
consumer health - Skin Cancer
.
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(PMID = 16456318.001).
[ISSN]
0193-1091
[Journal-full-title]
The American Journal of dermatopathology
[ISO-abbreviation]
Am J Dermatopathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta
100.
Wang HQ, Huang DS:
Non-linear cancer classification using a modified radial basis function classification algorithm.
J Biomed Sci
; 2005 Oct;12(5):819-26
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Non
-
linear
cancer
classification
using a modified radial basis function
classification
algorithm.
This paper proposes a modified radial basis function
classification
algorithm
for non
-
linear
cancer
classification
.
In the algorithm, a modified simulated annealing method is developed and combined with the
linear
least square and gradient paradigms to optimize the structure of the radial basis function (RBF) classifier.
The proposed algorithm can be adopted to perform
non
-
linear
cancer
classification
based on gene expression profiles and applied to two microarray data sets involving various human tumor classes:.
(2)
acute
myeloid
leukemia
(
AML
) versus
acute
lymphoblastic
leukemia
(ALL).
Finally, accuracy and stability for the proposed algorithm are further demonstrated by comparing with the other cancer
classification
algorithms.
[MeSH-major]
Algorithms. Colonic Neoplasms /
classification
.
Leukemia
,
Myeloid
/
classification
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
classification
[MeSH-minor]
Acute
Disease
. Humans
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(PMID = 16132112.001).
[ISSN]
1021-7770
[Journal-full-title]
Journal of biomedical science
[ISO-abbreviation]
J. Biomed. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
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